lipid-P Cancer Research Results

lipid-P, lipid peroxidation: Click to Expand ⟱

Source:

Type:

Lipid peroxidation is a chain reaction process in which free radicals (often reactive oxygen species, or ROS) attack lipids containing carbon-carbon double bonds, especially polyunsaturated fatty acids. This attack results in the formation of lipid radicals, peroxides, and subsequent breakdown products.
Lipid peroxidation can cause damage to cell membranes, leading to increased permeability and disruption of cellular functions. This damage can initiate a cascade of events that may contribute to carcinogenesis.
The byproducts of lipid peroxidation, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), can form adducts with DNA, leading to mutations. These mutations can disrupt normal cellular processes and contribute to the development of cancer.
Lipid peroxidation damages cell membranes, disrupts cellular functions, and can trigger inflammatory responses. It is a marker of oxidative stress and is implicated in many chronic diseases.

Negative Prognostic Indicator: In many cancers, high levels of lipid phosphates, particularly S1P, are associated with poor prognosis, indicating a more aggressive tumor phenotype and potential resistance to therapy.
Mixed Evidence: The prognostic significance of lipid phosphates can vary by cancer type, with some studies showing that their expression may not always correlate with adverse outcomes.

Scientific Papers found: Click to Expand⟱

6461-

1,8-Cin,

1,8-cineole (eucalyptol): A versatile phytochemical with therapeutic applications across multiple diseases

Review,

AD,

Review,

Var,

*Inflam↓, long history of use in traditional medicine and exhibits an array of biological properties, including anti-inflammatory, antioxidant, antimicrobial, bronchodilatory, analgesic, and pro-apoptotic effects.
*antiOx↑,
*neuroP↑, recent studies have highlighted the neuroprotective, analgesic, and pro-apoptotic properties of 1,8-cineole, underscoring its potential beneficial role in a broad spectrum of conditions such as Alzheimer’s disease, neuropathic pain, and cancer
*BioAv↑, Marked by a logP value of 2.74, 1,8-cineole strikes an optimal equilibrium between solubility and permeability, hinting at its favorable potential for oral bioavailability
*Half-Life↝, In rabbits, oral administration of 200 mg/kg has led to rapid attainment of peak plasma concentration within 1 h, indicating efficient absorption
*toxicity↓, compound’s toxicity profile, the oral acute LD50 value in rats is documented at 2480 mg/kg body weight
*PGE2↓, 1,8-cineole decreased the release of prostaglandin E2 and leukotriene B4 (LTB4) from peripheral blood mononuclear cells in asthmatic patients, and reduced TNF-α, IL-1β, LTB4, and thromboxane B2 in lipopolysaccharide (LPS)-stimulated peripheral blood
*TNF-α↓,
*IL1β↓,
*NO↓, 1,8-cineole hindered LPS-induced nitric oxide (NO) production in mouse macrophage cell lines
*NF-kB↓, inhibition of nuclear translocation of NF-κB p65 and PPARγ, leading to the suppression of immune response genes.
*PPARγ↓,
COX2↓, ,8-cineole has been found to impede UVB-induced COX-2 protein and mRNA production in HaCaT cells
*ROS↓, 1,8-cineole’s antioxidant properties play a crucial role in its therapeutic potential, as it is effective in neutralizing reactive oxygen species (ROS)
*SOD↑, 1,8-cineole treatment enhanced antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), increased total antioxidant capacity, and decreased ROS and malondialdehyde (MDA)
*Catalase↑,
*TAC↑,
*MDA↓,
*lipid-P↓, 1,8-cineole has demonstrated the ability to inhibit LP
*NRF2↑, The antioxidant activity of 1,8-cineole is mediated, in part, by activating the Nrf2/Keap1 system
*HO-1↑, increased expression of phase II detoxifying enzymes and antioxidant proteins, such as heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 (NOQ1)
*NADPH↑,
*GPx↑, 1,8-cineole treatment has been shown to enhance the activities of antioxidant enzymes, such as SOD, GPx, and CAT,
*AntiBio↑, Antibacterial properties: activity, synergy with antibiotics, and impact on biofilm formation and cell morphology
*eff↑, Although 1,8-cineole exhibited weaker bactericidal activity than commonly used antibiotics such as gentamicin and amoxicillin (AMX)/clavulanic acid, it significantly reduced the minimum inhibitory concentration of antibiotics when used in combination
*AntiFungal↑, Antifungal properties: inhibition of fungal growth and disruption of biofilm formation
*AntiViral↑, Antiviral properties: inhibition of viral replication and enhancement of antiviral responses
*TRPA1↑, 1,8-cineole could activate TRPA1 channels in the dorsal root ganglia (DRG),
eff↑, when combined with simvastatin, increased G0/G1 cell cycle arrest and sensitized cells to apoptosis
TumCCA↑, 1,8-cineole induced G0/G1 arrest and senescence in HepG2 cells through oxidative stress and various signaling pathways such as MAPK, AMPK, and Akt/mTOR
ROS↑,
MAPK↝,
mTOR↝,
Apoptosis↑, HCT116 and RKO human colon cancer cell lines, 1,8-cineole selectively promoted apoptosis rather than necrosis
survivin↓, This process was linked to survivin and Akt inactivation, along with p38 activation.
Akt↓,
p38↑,
cl‑PARP↑, triggered subsequent cleavage of PARP and caspase-3, resulting in apoptosis.
cl‑Casp3⇅,
P53↑, increasing p53 expression, as well as the expression of apoptotic proteins (Bax/Bcl-2, Cyt-c, caspase-9, and caspase-3)
BAX↑,
Cyt‑c↑,
Casp9↑,
Dose↝, efficacious concentrations of 1,8-cineole reported for inhibiting in vitro cancer cell proliferation range from micromolar [135], [136] to millimolar (mM)
*Aβ↓, 1,8-cineole in rat PC12 cells (pheochromocytoma cells) demonstrated effective mitigation of the Aβ induced cytotoxicity and oxidative stress
*tau↓, 1,8-cineole has shown the ability to modulate tau phosphorylation by suppressing GSK-3β activity and to reduce Aβ production by inhibiting beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), both in vitro and in vivo
*GSK‐3β↓,
*BACE↓,
*cardioP↑, 1,8-cineole enhanced cell viability, inhibited cardiac hypertrophy, attenuated cardiac remodeling, improved cardiac function, and decreased the concentrations of atrial natriuretic peptide and brain natriuretic peptide in rat hearts
MFN2↑, 1,8-cineole was also found to inhibit the activation of dynamin-related protein 1 and promote mitochondrial fusion by increasing MFN2.

6462-

1,8-Cin,

Modes of Action of 1,8-Cineol in Infections and Inflammation

Review,

Var,

Review,

AD,

*BioAv↑, become increasingly clear in the recent years that 1,8-Cineol spreads almost everywhere in the human body after its oral administration, from the gut to the blood to the brain.
*BBB↑,
*AntiViral↑, anti-viral effects have been observed to include numerous bacteria and fungi species.
*Bacteria↓,
*AntiFungal↑,
*Inflam↓, central mode of action of 1,8-Cineol is the inhibition of pro-inflammatory cytokine expression
*BioAv↑, 1,8-Cineol was detectable in nasal tissue samples after its oral administration for 14 days, which indicates the systemic distribution of 1,8-Cineol via the gut and the blood stream
*MUC2↓, significantly reduced expression levels of the mucin genes MUC2 and MUC19 in close association with a significantly attenuated activity of transcription factor NF-κB
*MUC19↓,
*NF-kB↓, reduced the expression levels of transcriptional activator nuclear factor (NF)-kB p65 and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in lung tissues
*ICAM-1↓,
*VCAM-1↓,
DNAdam↑, colon cancer cells on the potential genotoxicity of 1,8-Cineol revealed a concentration-dependent increase in oxidative DNA damage, whereas it did not affect the cell viability due to DNA repair mechanisms
*lipid-P↓, suppressing the expression of lipid mediators and prostaglandin D2
*PGE2↓,
*IL4↓, decreased expression levels of different inflammatory cytokines such as interleukin (IL)-4, IL-6 and granulocyte macrophage colony stimulating factor (GM-CSF) in bronchial epithelial cells
*IL6↓,
*IL1β↓, 1,8-Cineol-containing leaf extracts significantly suppressed the expression of pro-inflammatory cytokines IL-1β and IL-6 [
*IL6↓,
eff↑, 1,8-Cineol in combination with ellagic acid has been shown to downregulate different cytokines such as transforming growth factor beta-1 (TGF-β1), Fascin-1 (FSCN1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) in p
TGF-β↓,
fascin↓,
VEGF↓,
MMP9↓,
*MAPK↓, 1,8-Cineol was shown to suppress the activation of the MAPK/ERK
*ERK↓,
JNK↓, decreased activities of transcription factor NFκB and the JNK (c-Jun N-terminal kinase)/AP-1 (activator protein-1) pathway in the human cancer cell lines U373 and HeLa in response to 1,8-Cineol, the active ingredient of the drug Soledum
Wnt↓, 1,8-Cineol acts as an inhibitor of the Wnt/β-catenin pathway in head and neck squamous cell carcinoma (HNSCC).
β-catenin/ZEB1↓,
GSK‐3β↑, decreased inhibition of glycogen synthase kinase 3 (GSK-3) and reduced levels of WNT11
*neuroP↑, 1,8-Cineol has been shown to have neuroprotective activity.
*GSK‐3β↓, decreased activity of GSK-3 in response to 1,8-Cineol could ameliorate advanced glycation end products,
*AGEs↓,
*BBB↑, eucalyptol reveals an opening effect on the blood–brain barrier
*NLRP3↓, controls inflammation by suppressing the NOD-like receptor pyrin domain-containing 3 (NLRP3) activation

2656-

AL,

Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics

in-vitro,

Park,

PC12

*antiOx↑, Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies.
*Apoptosis↓, allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure
*LDH↓,
ROS↓, Allicin also inhibited ROS generation
*lipid-P↓, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities.
*mtDam↓, These protective effects were associated with suppressed mitochondrial dysfunction,
*MMP↓, as evidenced by decreased MMP collapse and cytochrome c release,
*Cyt‑c↓,
*ATP∅, preserved mitochondrial ATP synthesis,
*Ca+2↝, and the promotion of mitochondrial Ca(2+) buffering capacity
*neuroP↑, allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.

2660-

AL,

Allicin: A review of its important pharmacological activities

Review,

AD,

Review,

Var,

Review,

Park,

Review,

Stroke,

*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,

5355-

AL,

Mini-review: The health benefits and applications of allicin

Review,

Var,

*BioAv↑, another key property of allicin is its hydrophobicity, which allows it to be absorbed easily through the cell membrane without causing any physical or chemical damage to the phospholipid bilayer, thereby allowing its rapid metabolism to produce pharm
*cardioP↑, Allicin exhibits protective effects in multiple organ systems, including the brain, intestines, lungs, liver, kidneys, prostate, and heart.
*hepatoP↑,
*RenoP↑,
*Half-Life↝, half-life (t1/2)of allicin was 227 min–260 min. Because allicin is eliminated from the body by the respiratory tract, the concentration of allicin in lung tissue is significantly lower than that in the blood
*BioAv↓, We believe that the bioavailability of allicin is relatively low for the following reasons: At first, allicin is characterized by a distinctive garlic odor and chemical instability. It can be easily degraded under room temperature.
*neuroP↑, Neuroprotective activity
*cognitive↑, On the other hand, allicin improves cognitive deficits via Protein kinase R-like endoplasmic reticulum kinase (PERK)/Nuclear factor erythroid-2-related factor 2 (NRF2) signaling pathway and c-Jun N-terminal kinase (JNK) signaling pathways
*ROS↓, They found that allicin suppressed ROS generation and decreased lipid peroxidation in 6-hydroxydopamine (6-OHDA)-induced Pheochromocytoma 12 (PC12) cells
*lipid-P↓,
*DNArepair↑, Allicin not only directly protects DNA, but also indirectly protects DNA through antioxidant activity and regulation of oxidizing enzymes
*ChemoSen↑, Allicin combined with other chemotherapy drugs showed a better anti-cancer effect

4282-

ALA,

Effect of add-on alpha lipoic acid on psychopathology in patients with treatment-resistant schizophrenia: a pilot randomized double-blind placebo-controlled trial

Trial,

NA,

*antiOx↑, Alpha lipoic acid (ALA) is a naturally occurring antioxidant that plays an important role in the functioning of enzymes involved in mitochondrial oxidative metabolism
*Inflam↓, act as antioxidant and anti-inflammatory agents
*lipid-P↓, ALA supplementation has been shown to decrease lipid peroxidation in healthy controls but not in patients with schizophrenia
*adiP↑, ALA has also been shown to improve adiponectin levels, prevent weight gain or weight loss
*cognitive∅, no significant difference between placebo and the ALA groups in scores of cognitive functions
*BDNF↑, median BDNF levels increased from 5.06 to 5.50 ng/mL

297-

ALA,

Insights on the Use of α-Lipoic Acid for Therapeutic Purposes

Review,

BC,

SkBr3

Review,

neuroblastoma,

SK-N-SH

Review,

AD,

PDH↑, ALA is capable of activating pyruvate dehydrogenase in tumor cells.
TumCG↓, ALA also significantly inhibited tumor growth in mouse xenograft model using BCPAP and FTC-133 cells
ROS↑, ALA is able to generate ROS, which promote ALA-dependent cell death in lung cancer [75], breast cancer [76] and colon cancer
AMPK↑,
EGR4↓,
Half-Life↓, Data suggests that ALA has a short half-life and bioavailability (about 30%)
BioAv↝,
*GSH↑, Moreover, it is able to increase the glutathione levels inside the cells, that chelate and excrete a wide variety of toxins, especially toxic metals from the body
*IronCh↑, The existence of thiol groups in ALA is responsible for its metal chelating abilities [14,35].
*ROS↓, ALA exerts a direct impact in oxidative stress reduction
*antiOx↑, ALA is being referred as the universal antioxidant
*neuroP↑, ALA has neuroprotective effects on Aβ-mediated cytotoxicity
*Ach↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*lipid-P↓, ALA has multiple and complex effects in this way, namely scavenging ROS, transition metal ions, increasing the levels of reduced glutathione [59,63], scavenging of lipid peroxidation products
*IL1β↓, ALA downregulated the levels of the inflammatory cytokines IL-1B and IL-6 in SK-N-BE human neuroblastoma cells
*IL6↓,
TumCP↓, ALA inhibited cell proliferation, [18F]-FDG uptake and lactate formation and increased apoptosis in neuroblastoma cell lines Kelly, SK-N-SH, Neuro-2a and in the breast cancer cell line SkBr3.
FDG↓,
Apoptosis↑,
AMPK↑, ALA suppressed thyroid cancer cell proliferation and growth through activation of AMPK and subsequent down-regulation of mTOR-S6 signaling pathway in BCPAP, HTH-83, CAL-62 and FTC-133 cells lines.
mTOR↓,
EGFR↓, ALA inhibited cell proliferation through Grb2-mediated EGFR down-regulation
TumCI↓, ALA inhibited metastatic breast cancer cells migration and invasion, partly through ERK1/2 and AKT signaling
TumCMig↓,
*memory↑, Alzheimer’s Disease: ALA led to a marked improvement in learning and memory retention
*BioAv↑, Since ALA is poorly soluble, lecithin has been used as an amphiphilic matrix to enhance its bioavailability.
*BioAv↝, ALA were found to be considerably higher in adults with mean age greater than 75 years as compared to young adults between the ages of 18 and 45 years.
*other↓, ALA treatment has been recently studied by some clinical trials to explain its efficacy in preventing miscarriage
*other↝, 1800 mg of ALA or placebo were administrated orally every day, except during the period 2 days before to 4 days after administration of each dose of platinum to avoid potential interference with platinum’s antitumor effects
*Half-Life↓, Data shows a short half-life and bioavailability of about 30% of ALA due to mechanisms involving hepatic degradation, reduced ALA solubility as well as instability in the stomach.
*BioAv↑, ALA bioavailability is greatly reduced after food intake and it has been recommended that ALA should be admitted at least 2 h after eating or if taken before; meal should be taken at least 30 min after ALA administration
*ChAT↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*GlucoseCon↑,

3269-

ALA,

Sulfur-containing therapeutics in the treatment of Alzheimer’s disease

NA,

AD,

*AChE↓, ALA activated AChE and increased glucose uptake, thus providing more acetyl-CoA to generate acetylcholine (ACh). (note activated AChE in this review likely should say inhibited!!!)
*GlucoseCon↑,
*ACC↑,
*GSH↑, ALA increased intracellular GSH levels by chelating redox-active transition metals, thus inhibiting the formation of hydroxyl radicals and Aβ aggregation.
*Aβ↓,
*Catalase↑, Levels of several antioxidant enzymes including catalase, GR, glutathione-S-transferase (GST), NADPH, and quinone oxidoreductase-1 (NQO1) were enhanced by ALA
*GSR↑,
*GSTs↑,
*NADPH↑,
*NQO1↑,
*iNOS↓, LA prevented the induction of iNOS, inhibited TNFα-induced activation of NF-κB [42], levels of which are increased in AD.
*NF-kB↓,
*lipid-P↓, ALA reduced the levels of lipid peroxidation products
*BBB↑, ALA could easily cross the blood–brain barrier (BBB)
*memory↑, ALA treatment significantly improved the spatial memory and cognition capacity of the mice in the Morris water maze and novel object recognition test.
*cognitive↑,
*antiOx↑, antioxidant and anti-inflammatory activities of ALA
*Inflam↓,

3438-

ALA,

The Potent Antioxidant Alpha Lipoic Acid

Review,

NA,

Review,

AD,

*antiOx↑, Both of alpha lipoic acid and its reduced form have been shown to possess anti-oxidant, cardiovascular, cognitive, anti-ageing, detoxifying, anti-inflammatory, anti-cancer, and neuroprotective pharmacological properties
*cardioP↑,
*cognitive↑, Alpha lipoic acid has the ability to decrease cognitive impairment and may be a successful therapy for Alzheimer’s disease and any disease related dementias
*AntiAge↑,
*Inflam↓,
*AntiCan↑,
*neuroP↑, ALA has neuroprotective effects in experimental brain injury caused by trauma and subarachnoid hemorrhage
*IronCh↑, Also, the ability of ALA to chelate metals can produce an antioxidant effect
*ROS↑, DHLA can exert a pro-oxidant effect of donating its electrons for the reduction of iron, which can then break down peroxide to the prooxidant hydroxyl radical via the Fenton reaction [10]. So, ALA and its reduced form DHLA, can promote antioxidant pr
*Weight↓, α-lipoic acid supplementation at a dose of 300 mg/day might help to could help to promote weight loss and fat mass reduction in healthy overweight/obese women following an energy-restricted balanced diet
*Ach↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*ROS↓, also scavenges reactive oxygen species, thereby increasing the concentration levels of reduced Glutathione (GSH).
*GSH↑,
*lipid-P↓, Alpha lipoic acid can scavenge lipid peroxidation products as hydroxynonenal and acrolein.
*memory↑, learning and memory in the passive avoidance test partially through its antioxidant activity.
*NRF2↑, α-LA treatment has been shown to increase Nrf2 nuclear localization
*ChAT↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*GlucoseCon↑,
*Acetyl-CoA↑,

3540-

ALA,

Thioctic (lipoic) acid: a therapeutic metal-chelating antioxidant?

in-vitro,

NA,

*lipid-P↓, TA also inhibited Cu(2+)-catalysed liposomal peroxidation.
*H2O2↓, TA inhibited intracellular H2O2 production in erythrocytes challenged with ascorbate,
*IronCh↑, ability of TA to act as a metal-chelator

3543-

ALA,

The Effect of Lipoic Acid Therapy on Cognitive Functioning in Patients with Alzheimer's Disease

Study,

AD,

600 mg/day

 126 patients (75 women and 51 men) with AD

*cognitive↑, Our study suggests that ALA therapy could be effective in slowing cognitive decline in patients with AD and IR.
*antiOx↑, Alpha-lipoic acid (ALA) is a naturally occurring disulfide molecule with antioxidant and anti-inflammatory properties.
*Inflam↓,
*neuroP↑, ALA plays many different roles in pathogenic pathways of dementia, acting as a neuroprotective agent.
*Ach↑, It increases acetylcholine production, inhibits hydroxyl radical production, and increases the process of getting rid of reactive oxygen species.
*ROS↓,
*GlucoseCon↑, (ii) increased glucose uptake, supplying more acetyl-CoA for the production of Ach;
*lipid-P↓, (v) scavenging lipid peroxidation products;
*GSH↑, (vi) inducing enzymes of glutathione synthesis
*Acetyl-CoA↑,

3547-

ALA,

Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

Review,

AD,

Review,

Park,

*memory↑, a number of preclinical studies showing beneficial effects of LA in memory functioning, and pointing to its neuroprotective potential effect
*neuroP↑,
*motorD↑, Improved motor dysfunction
*VitC↑, elevates the activities of antioxidants such as ascorbate (vitamin C), α-tocoferol (vitamin E) (Arivazhagan and Panneerselvam, 2000), glutathione (GSH)
*VitE↑,
*GSH↑,
*SOD↑, superoxide dismutase (SOD) activity (Arivazhagan et al., 2002; Cui et al., 2006; Militao et al., 2010), catalase (CAT) (Arivazhagan et al., 2002; Militao et al., 2010), glutathione peroxidase (GSH-Px)
*Catalase↑,
*GPx↑,
*5HT↑, ↑levels of neurotransmitters (dopamine, serotonin and norepinephrine) in various brain regions
*lipid-P↓, ↓ level of lipid peroxidation,
*IronCh↑, ↓cerebral iron levels,
*AChE↓, ↓ AChE activity, ↓ inflammation
*Inflam↓,
*GlucoseCon↑, ↑brain glucose uptake; ↑ in the total GLUT3 and GLUT4 in the old mice;
*GLUT3↑,
*GLUT4↑,
NF-kB↓, authors showed that LA inhibited the stimulation of nuclear factor-κB (NF-κB)
*IGF-1↑, LA restored the parameters of total homocysteine (tHcy), insulin, insulin like growth factor-1 (IGF-1), interlukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Mahboob et al. (2016), analyzed the effects of LA in AlCl3- model of neurodegeneration,
*IL1β↓,
*TNF-α↓, Suppression of NF-κβ p65 translocation and production of proinflammatory cytokines (IL-6 and TNF-α) followed inhibition of cleaved caspase-3
*cognitive↑, demonstrating its capacity in ameliorating cognitive functions and enhancing cholinergic system functions
*ChAT↑, LA treatment increased the expression of muscarinic receptor genes M1, M2 and choline acetyltransferase (ChaT) relative to AlCl3-treated group.
*HO-1↑, R-LA and S-LA also enhanced expression of genes related to anti-oxidative response such as heme oxygenase-1 (HO-1) and phase II detoxification enzymes such as NAD(P)H:Quinone Oxidoreductase 1 (NQO1).
*NQO1↑,

3546-

ALA,

Cognitive and Mood Effect of Alpha-Lipoic Acid Supplementation in a Nonclinical Elder Sample: An Open-Label Pilot Study

Study,

AD,

fifteen elder patients (mean age: 84.5 ± 5.77) received ALA at a daily dose of 600 mg/day for 12 weeks.

*antiOx↑, (ALA), a known antioxidant compound abundant in vegetables and animal tissues, in reducing oxidative stress in the aging brain and preventing cognitive decline.
*ROS↓,
*cognitive∅, no statistically significant effects either on cognitive function, executive function, or mood were found
*lipid-P↓, ALA has been shown to reduce lipid peroxidation and increase the activity of antioxidant molecules in different areas of the brain of experimental animals
*memory↑, ALA has been suggested to improve memory by increasing the activity of choline acetyltransferase (ChAT)
*ChAT↑,
*Acetyl-CoA↑, a crucial step in the biosynthesis of acetylcholine, in the hippocampi of treated rats
*Aβ↓, ALA administration can inhibit the formation of beta-amyloid fibrils and their expansion, thus exerting a direct effect on a known mechanism involved in neurodegenerative diseases
*BioAv↑, ALA is abundantly present in vegetables and animal tissues [17], is promptly bioavailable, and has no known toxic effects on animals and human subjects
*BBB↑, ALA has been demonstrated to successfully cross the blood–brain barrier in animal models
*toxicity∅, and no collateral effects have been observed at the oral daily doses currently employed as supplements (from 50 to 2400 mg/day)

3545-

ALA,

Potential therapeutic effects of alpha lipoic acid in memory disorders

Review,

AD,

*neuroP↑, potential therapeutic effects for the prevention or treatment of neurodegenerative disease
*Inflam↓, ALA is able to regulate inflammatory cell infiltration into the central nervous system and to down-regulate VCAM-1 and human monocyte adhesion to epithelial cells
*VCAM-1↓, down-regulate vascular cell adhesion molecule-1 (VCAM-1) and the human monocyte adhesion to epithelial cells
*5HT↑, ALA is able to improve the function of the dopamine, serotonin and norepinephrine neurotransmitters
*memory↑, scientific evidence shows that ALA possesses the ability to improve memory capacity in a number of experimental neurodegenerative disease models and in age-related cognitive decline in rodents
*BioAv↝, Between 27 and 34% of the oral intake is available for tissue absorption; the liver is one of the main clearance organs on account of its high absorption and storage capacity
*Half-Life↓, The plasma half-life of ALA is approximately 30 minutes. Peak urinary excretion occurs 3-6 hours after intake.
*NF-kB↓, As an inhibitor of NF-κβ, ALA has been studied in cytokine-mediated inflammation
*antiOx↑, In addition to the direct antioxidant properties of ALA, some studies have shown that both ALA and DHLA and a great capacity to chelate redox-active metals, such as copper, free iron, zinc and magnesium, albeit in different ways (
*IronCh↑, ALA is able to chelate transition metal ions and, therefore, modulate the iron- and copper-mediated oxidative stress in Alzheimer’s plaques
*ROS↓, iron and copper chelation with DHLA may explain the low level of free radical damage in the brain and the improvement in the pathobiology of Alzheimer’s Disease
*ATP↑, ALA may increase the mitochondrial synthesis of ATP in the brain of elderly rats, thereby increasing the activity of the mitochondrial enzymes
*ChAT↑, ALA may also play a role in the activation of the choline acetyltransferase enzyme (ChAT), which is essential in the anabolism of acetylcholine
*Ach↑,
*cognitive↑, One experimental study has shown that in rats that had been administered ALA there was an inversion in the cognitive dysfunction with an increase in ChAT activity in the hippocampus
*lipid-P↓, administration of ALA reduces lipid peroxidation in different areas of the brain and increases the activity of antioxidants such as ascorbate (vitamin C), α-tocopherol (vitamin E), glutathione,
*VitC↑,
*VitE↑,
*GSH↑,
*SOD↑, and also the activity of superoxide dismutase, catalase, glutathione-peroxidase, glutathione-reductase, glucose-6-P-dehydrogenase
*Catalase↑,
*GPx↑,
*Aβ↓, Both ALA and DHLA have been seen to inhibit the formation of Aβ fibrils

3676-

Ash,

Effect of Withania somnifera (Ashwagandha) root extract on amelioration of oxidative stress and autoantibodies production in collagen-induced arthritic rats

in-vivo,

Arthritis,

(100, 200, 300 mg/kg b. wt., orally)

arthritic rats

*CRP↓, WSAq resulted in a dose-dependent reduction in arthritic index, autoantibodies and CRP
*ROS↓, oxidative stress in CIA rats was ameliorated by treatment with different doses of WSAq, as evidenced by a decrease in lipid peroxidation and glutathione-S-transferase activity and an increase in the glutathione
*lipid-P↓,
*GSTs↓,
*GSH↑,
*antiOx↑, WSAq exhibited antioxidant and anti-arthritic activity and reduced inflammation in CIA rats
*Inflam↓,

3669-

Ash,

Withanamides in Withania somnifera fruit protect PC-12 cells from beta-amyloid responsible for Alzheimer's diseas

in-vitro,

AD,

PC12

*lipid-P↓, Withania somnifera fruit afforded lipid peroxidation inhibitory withanamides that are more potent than the commercial antioxidants.
*antiOx↑,

3162-

Ash,

Molecular insights into cancer therapeutic effects of the dietary medicinal phytochemical withaferin A

Review,

Var,

lipid-P↓, Oral cancer 20 mg/Kg ↓Lipid peroxidation : ↑SOD, glutathione peroxidase, p53, Bcl-2
SOD↑,
GPx↑,
P53↑,
Bcl-2↑,
E6↓, Cervival cancer 8mg/Kg ↓E6, E7: ↑p53, pRb, Cyclin B1, P34 Cdc2, p21, PCNA
E7↓,
pRB↑,
CycB/CCNB1↑,
CDC2↑,
P21↑,
PCNA↓,
ALDH1A1↓, Mammary cancer 0-1 mg/mouse (5-10) ↓Mammosphere number, ALDH1 activity. Vimentin, glycolysis
Vim↓,
Glycolysis↓,
cMyc↓, Mesotheliome cancer 5 mg/Kg ↓Proteasomal chymotrypsin, C-Myc : ↑ Bax, CARP-1
BAX↑,
NF-kB↓,
Casp3↑, caspase-3 activation
CHOP↑, WA is found to increase activation of Elk1 and CHOP (CCAAT-enhancer-binding protein homologous protein) by RSK, as well as up-regulation of DR5 by selectively suppressing pathway ERK
DR5↑,
ERK↓,
Wnt↓, WA inhibits Wnt/Î²-catenin pathway via suppression of AKT signalling, which inhibits cancer cell motility and sensitises for cell death
β-catenin/ZEB1↓,
Akt↓,
HSP90↓, WA-dependent inhibition of heat shock protein (HSP) chaperone functions. WA inhibits the activity of HSP90-mediated function

4303-

Ash,

Ashwagandha (Withania somnifera)—Current Research on the Health-Promoting Activities: A Narrative Review

Review,

AD,

*neuroP↑, neuroprotective, sedative and adaptogenic effects and effects on sleep.
*Sleep↑,
*Inflam↓, anti-inflammatory, antimicrobial, cardioprotective and anti-diabetic properties
*cardioP↑,
*cognitive↑, Significant improvements in cognitive function were observed as a result of the inhibition of amyloid β-42, and a reduction in pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and MCP-1, nitric oxide, and lipid peroxidation was also observed.
*Aβ↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*MCP1↓,
*lipid-P↓,
*tau↓, reducing β-amyloid aggregation and inhibiting τ protein accumulation.
*ROS↓, withaferin A is responsible for inhibiting oxidative and pro-inflammatory chemicals and regulating heat shock proteins (HSPs), the expression of which increases when cells are exposed to stressors.
*BBB↑, ability of withanolide A to penetrate the blood-brain barrier (BBB) was demonstrated.
*AChE↓, potentially inhibiting acetylcholinesterase activity, which may have benefits in the treatment of canine cognitive dysfunction and Alzheimer’s disease
*GSH↑, increased glutathione concentration, increased glutathione S-transferase, glutathione reductase, glutathione peroxidase, superoxide dismutase and catalase activities,
*GSTs↑,
*GSR↑,
*GPx↑,
*SOD↑,
*Catalase↑,
ChemoSen↑, combination of Ashwagandha extract and intermittent fasting has potential as an effective breast cancer treatment that may be used in conjunction with cisplatin
*Strength↑, combination of Ashwagandha extract and intermittent fasting has potential as an effective breast cancer treatment that may be used in conjunction with cisplatin

5427-

ASTX,

Astaxanthin and Cancer Chemoprevention

Review,

Var,

chemoP↑, evidence for anticarcinogenic behavior of selected carotenoids, with an emphasis on the chemopreventive activities of astaxanthin.
AntiCan↑, Human epidemiological studies have revealed a protective effect of vegetable and fruit consumption for cancers of the stomach, esophagus, lung, oral cavity and pharynx, bladder, endometrium, pancreas, colon and rectum, breast, cervix, ovary and prost
chemoPv↑, the chemopreventive effects of canthaxanthin
Risk↓, Salmon, the principal dietary source of astaxanthin, is an important component of the traditional diets of Eskimos and certain coastal tribes in North America; these groups have shown unusually low prevalence of cancer.
lipid-P↓, Dietary astaxanthin also reduced metastatic nodules and lipid peroxidation in the livers of rats treated with restraint stress.
Pain↓, The results revealed that astaxanthin significantly relieved pain and improved performance in patients with RA
BioAv↑, the results demonstrated an enhancement of astaxanthin bioavailability in humans when incorporated into lipid-based formulations.
Dose↝, relevant dietary dosages of astaxanthin (4-12 mg daily is typically recommended by supplement manufacturers),

5419-

ASTX,

Astaxanthin and other Nutrients from Haematococcus pluvialis—Multifunctional Applications

Review,

Nor,

*antiOx↑, extraction of astaxanthin and analysis of its antioxidant, anti-inflammatory, anti–diabetic and anticancer activities.
*Inflam↓,
*AntiDiabetic↓,
AntiCan↑,
*lipid-P↓, astaxanthin is more effective than β-carotene in the prevention of lipid peroxidation.
TumCP↓, Studies have reported that astaxanthin not only inhibits the proliferation of colon cancer cells but can also cause their apoptosis
Apoptosis↑,
TumCCA↑, Astaxanthin was included in the extract and was responsible for stopping the progression of the cell cycle and promoting the apoptosis [95].
*SOD↑, Astaxanthin also increased SOD activity and decreased PG-E2, LT-B4, NO, IL-8 and IFN- γ production [103,104,105].
*PGE2↓,
*NO↓,
*IL8↓,
*IFN-γ↓,
*cardioP↑, Astaxanthin has a cardiovascular protective effect in animals, but there is a lack of research supporting the therapeutic benefit of astaxanthin in atherosclerotic cardiovascular disease in humans.
*NF-kB↓, Oral supplementation with astaxanthin in rats after surgery decreased the expression of NF-KB and TNF-α,
*TNF-α↓,
*BioAv↑, Satisfactory astaxanthin bioavailability results were obtained with a daily astaxanthin dose of 40 mg/day.

5449-

ATV,

Pleiotropic effects of statins: A focus on cancer

NA,

Var,

lipid-P↓, Statins exhibit “pleiotropic” properties that are independent of their lipid-lowering effects.
TumCG↓, preclinical evidence suggests that statins inhibit tumor growth and induce apoptosis in specific cancer cell types.
Apoptosis↑,
ChemoSen↑, statins show chemo-sensitizing effects by impairing Ras family GTPase signaling.
RAS↓,
HMG-CoA↓, Statins are potent, competitive inhibitors of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase (HMGCR).
HMGCR↓,
LDL↓, Statins reduce blood plasma cholesterol levels by decreasing de novo cholesterol biosynthesis and by inducing changes in low density lipoprotein (LDL) receptor expression [2].
toxicity↓, Due to the well-established safety profile of statins, such studies are less expensive than the development of novel drugs.
Risk↓, statin use in cancer patients was associated with reduced cancer-related mortality. The risk of cancer death was significantly lower in postmenopausal women
P21↑, Other proposed mechanisms leading to an increase of p21 levels include the release of promoter-associated histone deacetylase and inhibition of histone deacetylase
HDAC↓,
Bcl-2↓, Statins trigger the intrinsic apoptosis pathway and decrease Bcl-2 protein expression [[154], [155], [156]], increase Bax and BIM protein expression [[156], [157], [158], [159]], and activate several caspases
BAX↑,
BIM↑,
Casp↑,
cl‑PARP↑, thereby increasing cleaved PARP-1 levels.
MMP↓, different tumor cell lines (breast, brain, and lung) showed that simvastatin-induced apoptosis is dependent on decreasing mitochondrial membrane potential and increasing reactive oxygen species (ROS) production
ROS↑,
angioG↓, Statins inhibit angiogenesis and metastasis
TumMeta↓,
PTEN↑, n breast cancer xenografts, simvastatin prevented tumor growth by reducing Akt phosphorylation and BclXL transcription, while simultaneously increasing the transcription of pro-apoptotic/anti-proliferative PTEN
eff↑, In mice, the administration of a combination of celecoxib and atorvastatin was more effective than each individual treatment, and effectively prevented prostate cancer progression from androgen dependent to androgen independent
OS↑, Long-term statin use may improve survival in GBM patients treated with temozolomide chemotherapy
Remission↑, statin use during or after chemotherapy is not associated with improved disease-free-, recurrence-free-, or overall survival in stage II colon cancer patients

5365-

AV,

Aloe Vera Polysaccharides as Therapeutic Agents: Benefits Versus Side Effects in Biomedical Applications

Review,

Nor,

Review,

IBD,

Review,

Diabetic,

*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].

2625-

Ba,

LT,

Baicalein and luteolin inhibit ischemia/reperfusion-induced ferroptosis in rat cardiomyocyte

in-vivo,

Stroke,

rat

*lipid-P↓, Baicalein and luteolin prevented the Fe-SP-induced lipid peroxidation in rat neonatal cardiomyocytes.
*ACSL4∅, Baicalein and luteolin can reduce the protein levels of ACSL4 and Nrf2, and enhance the protein levels of GPX4 in ischemia/reperfusion-treated rat hearts.
*NRF2∅, Our results suggest that BAI and Lut prevented the I/R-induced increased of ACSL4, NRF2, and HO-1 protein
*GPx4∅, BAI and Lut prevented the I/R-induced increased of ACSL4, NRF2, and HO-1 protein, and the I/R-decreased GPX4 protein levels
*Ferroptosis↓, BAI was found to suppress ferroptosis in cancer cells via reducing reactive oxygen species (ROS) generation.
*ROS↓,
*MDA↓, Moreover, both BAI and Lut decreased ROS and malondialdehyde (MDA) generation and the protein levels of ferroptosis markers, and restored Glutathione peroxidase 4 (GPX4) protein levels in cardiomyocytes reduced by ferroptosis inducers
*eff↑, BAI and Lut reduced the I/R-induced myocardium infarction
*HO-1∅, Our results suggest that BAI and Lut prevented the I/R-induced increased of ACSL4, NRF2, and HO-1 protein

2626-

Ba,

Molecular targets and therapeutic potential of baicalein: a review

Review,

Var,

Review,

AD,

Review,

Stroke,

AntiCan↓, anticancer, antidiabetic, antimicrobial, antiaging, neuroprotective, cardioprotective, respiratory protective, gastroprotective, hepatic protective, and renal protective effects
*neuroP↑,
*cardioP↑, Cardioprotective action of baicalein
*hepatoP↑,
*RenoP↑, baicalein’s capacity to lessen cisplatin-induced nephrotoxicity is probably due, at least in part, to the attenuation of renal oxidative and/or nitrative stress
TumCCA↑, Baicalein induces G1/S arrest in lung squamous carcinoma (CH27) cells by downregulating CDK4 and cyclin D1, as well as upregulating cyclin E
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↑,
BAX↑, SGC-7901 cells showed that when baicalein was administered, Bcl-2 was downregulated and Bax was increased
Bcl-2↓,
VEGF↓, Baicalein inhibits the synthesis of vascular endothelial growth factor (VEGF), HIF-1, c-Myc, and nuclear factor kappa B (NF-κB) in the G1 and S phases of ovarian cancer cell
Hif1a↓,
cMyc↓,
NF-kB↓,
ROS↑, Baicalein produced intracellular reactive oxygen species (ROS) and activated BNIP3 to slow down the development and hasten the apoptosis of MG-63,OS cell
BNIP3↑,
*neuroP↑, Baicalein exhibits neuroprotective qualities against amyloid (AN) functions by preventing AN from aggregating in PC12 neuronal cells to cause A𝛽-induced cytotoxicity
*cognitive↑, baicalein encourages non-amyloidogenic processing of APP, which lowers the generation of A𝛽 and enhances cognitive function
*NO↓, baicalein effectively reduced NO generation and iNOS gene expression
*iNOS↓,
*COX2↓, Baicalein therapy significantly decreased the expression of COX-2 and iNOS, as well as PGE2 and NF-κB, indicating a protective effect against cerebral I/R injury.
*PGE2↓,
*NRF2↑, Baicalein therapy markedly elevated nuclear Nrf2 expression and AMPK phosphorylation in the ischemic cerebral cortex
*p‑AMPK↑,
*Ferroptosis↓, Baicalein suppressed ferroptosis associated with 12/15-LOX, hence lessening the severity of post-traumatic epileptic episodes generated by FeCl3
*lipid-P↓, HT22 cells were damaged by ferroptosis, which is mitigated by baicalein may be due to its lipid peroxidation inhibitor
*ALAT↓, Baicalin lowers the raised levels of hepatic markers alanine transaminase (ALT), aspartate aminotransferase (AST)
*AST↓,
*Fas↓, Baicalin has also been shown to suppress apoptosis, decrease FAS protein expression, block the caspase-8 pathway, and decrease Bax protein production
*BAX↓,
*Apoptosis↓,

2689-

BBR,

Berberine protects against glutamate-induced oxidative stress and apoptosis in PC12 and N2a cells

in-vitro,

Nor,

PC12

in-vitro,

AD,

in-vitro,

Stroke,

*ROS↓, In both cell lines, pretreatment with berberine (especially at low concentrations) significantly decreased ROS generation, lipid peroxidation, and DNA fragmentation, while improving glutathione content and SOD activity in glutamate-injured cells.
*lipid-P↓,
*DNAdam↓, Berberine significantly diminished glutamate-induced DNA fragmentation
*GSH↑,
*SOD↑,
*eff↑, This is relevant to berberine treatment in neurodegenerative disorders, such as dementia (Alzheimer’s disease), seizures, and stroke.
*cl‑Casp3↓, Berberine significantly decreased cleaved caspase-3 and bax/bcl-2 expressions in the glutamate-injured cells
*BAX↓,
*neuroP↑, the current study demonstrated that berberine exerts neuroprotective effects against glutamate-induced N2a and PC12 cytotoxicity via antioxidant and anti-apoptotic mechanisms
*Dose↝, the protective effect of berberine was more significant at lower concentrations and decreased with increasing concentration.
*Ca+2↓, Nadjafi et al demonstrated that berberine protects OLN-93 oligodendrocytes against ischemic-induced cell death by attenuating the intracellular Ca2+ overload similar to the NMDA or the AMPA/kainate receptors antagonists

3677-

BBR,

Berberine: A Potential Multipotent Natural Product to Combat Alzheimer’s Disease

Review,

AD,

0.44uM(AChEi)

*antiOx↑, multiple activities of berberine, including antioxidant, acetylcholinesterase and butyrylcholinesterase inhibitory,
*AChE↓, inhibit AChE with an IC50 of 0.44 μM
*BChE↓, BChE inhibitor and the corresponding IC50 was estimated to be 3.44 μM
*MAOA↓, inhibitory activity on MAO-A with an IC50 value of 126 μM
*Aβ↓, monoamine oxidase inhibitory, amyloid-b peptide level-reducing and cholesterol-lowering activities.
*LDL↓, effectively reduce serum cholesterol and LDL-cholesterol levels in hyperlipidemic hamsters and human hypercholesterolemic patients
*ROS↓, First, it was reported that berberine can scavenge reactive oxygen species (ROS) and reactive nitrogen species (RNS)
*RNS↓,
*lipid-P↓, Secondly, berberine can inhibit lipid peroxidation
*Dose↝, berberine can inhibit AChE with an IC50 of 0.44 μM
*MAOB↓, inhibition of berberine against MAO-B: IC50 was estimated to be 98.4 μM
*memory↑, beneficial effect of berberine in ameliorating memory dysfunction in a rat model of streptozotocin-induced diabetes
*toxicity↓, Berberine is generally considered to be non-toxic at doses used in clinical situations and lacks genotoxic, cytotoxic or mutagenic activity
*BBB↑, Berberine can be administered orally [67] and pass through the blood-brain barrier

3679-

BBR,

Berberine alleviates Alzheimer's disease by activating autophagy and inhibiting ferroptosis through the JNK-p38MAPK signaling pathway

in-vivo,

AD,

5xFAD mice

*Beclin-1↑, autophagy-related markers Beclin1 and LC3B were upregulated and P62 was downregulated after BBR treatment.
*LC3B↑,
*p62↓,
*ROS↓, ROS and lipid peroxide MDA decreased significantly after BBR treatment.
*lipid-P↓,
*MDA↓,
*Ferroptosis↓, expression levels of ferroptosis-related genes TFR1, ASCL4, DMT1, and IREB2 were decreased, while the expression levels of FTH1 and SLC7A11 increased after BBR treatment.
*TfR1/CD71↓,
*FTH1↑,
*memory↑, BBR treatment enhanced spatial memory impairment in 5xFAD mice.
*JNK↓, inhibited ferroptosis by inhibiting the JNK-P38MAPK signaling pathway.
*p38↓,
*Aβ↓, further reducing Aβ plaque deposition, inhibiting inflammatory response,
*Inflam↓,

3682-

BBR,

Berberine Improves Cognitive Impairment by Simultaneously Impacting Cerebral Blood Flow and β-Amyloid Accumulation in an APP/tau/PS1 Mouse Model of Alzheimer’s Disease

in-vitro,

AD,

mouse

*cognitive↑, results showed that BBR ameliorated cognitive deficits in 3×Tg AD mice, reduced the Aβ accumulation, inhibited the apoptosis of neurons
*Aβ↓,
*Apoptosis↓,
*CD31↑, promoted the formation of microvessels in the mouse brain by enhancing brain CD31, VEGF, N-cadherin, Ang-1.
*VEGF↑,
*N-cadherin↑,
*angioG↑,
*neuroP↑, berberine is effective to 3×Tg AD mice, has a neuroprotective effect,
*p‑tau↓, lowering Aβ levels, inhibiting the phosphorylation of Tau protein, anti-oxidation, inhibiting the activity of AchE and MAO, and regulating lipids, hypoglycemic.
*antiOx↑,
*AChE↓,
*MAOB↓,
*lipid-P↓,

3684-

BBR,

Neuroprotective effects of berberine in animal models of Alzheimer’s disease: a systematic review of pre-clinical studies

Review,

AD,

*Inflam↓, berberine showed significant memory-improving activities with multiple mechanisms, such as anti-inflammation, anti-oxidative stress, cholinesterase (ChE) inhibition and anti-amyloid effects.
*antiOx↓,
*AChE↓,
*BChE↓, berberine exerts inhibitory effects on the four key enzymes in the pathogenesis of AD: acetylcholinesterase, butyrylcholinesterase, monoamine oxidase A, and monoamine oxidase B
*MAOA↓,
*MAOB↓,
*lipid-P↓, Fig3
*GSH↑,
*ROS↓,
*APP↓,
*BACE↓,
*p‑tau↓,
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*MAPK↓,
*PI3K↓,
*Akt↓,
*neuroP↑, neuroprotective effects of berberine have been extensively studied
*memory↑, berberine displayed significant effects in preventing memory impairment in these mechanistically different animal models, suggesting an over-all improvement of memory function by berberine

4299-

BBR,

Berberine attenuates cognitive impairment and ameliorates tau hyperphosphorylation by limiting the self-perpetuating pathogenic cycle between NF-κB signaling, oxidative stress and neuroinflammation

in-vivo,

AD,

AD mice

*memory↑, BBR improved learning and memory in APP/PS1 mice.
*p‑tau↓, BBR decreased the hyperphosphorylated tau protein in the hippocampus of APP/PS1 mice.
*NF-kB↓, BBR lowered the activity of NF-κB signaling in the hippocampus of AD mice.
*GSH↑, BBR-administration promoted the activity of glutathione (GSH) and inhibited lipid peroxidation in the hippocampus of AD mice.
*lipid-P↓,
*cognitive↑, BBR attenuated cognitive deficits and limited hyperphosphorylation of tau via inhibiting the activation of NF-κB
*ROS↓, by retarding oxidative stress and neuro-inflammation.
*Inflam↓,

5633-

BCA,

Mechanisms Behind the Pharmacological Application of Biochanin-A: A review

Review,

Var,

Review,

AD,

*AntiDiabetic↑, Through modulating oxidative stress, SIRT-1 expression, PPAR gamma receptors, and other multiple mechanisms biochanin-A produces anti-diabetic action.
*neuroP↑, Biochanin-A has been shown to have a potential neuroprotective impact by modulating multiple critical neurological pathways.
*toxicity↓, Unlike chemical agents such as chemotherapeutic agents, isoflavones have shown zero toxicity to humans
*CYP19↓, Biochanin-A inhibits CYP19 and negatively affects the synthesis of oestrogen in the body which enhances the anti-oestrogenic property in hormone-influenced cancer such as prostate cancer and breast cancer
p‑Akt↓, Biochanin-A inhibits Akt phosphorylation thereby downregulates mTOR signals and disrupts the cell cycle.
mTOR↓,
TumCCA↑,
P21↑, Biochanin-A cause apoptosis in lung cancer by increasing p21, caspase-3, and Bcl-2 levels. It lowers E-cadherin and blocks metastasis.
Casp3↑,
Bcl-2↑,
Apoptosis↑,
E-cadherin↓,
TumMeta↓,
eff↑, The synergism of biochanin-A with 5-fluorouracil evidenced in Caco-2 and HCT-116 cell lines indicates the modulatory influence of biochanin-A in colon cancer treatment.
GSK‐3β↓, It blocked the “Akt and GSK3β phosphorylation and boosted the degradation of β-catenin” ( Mahmoud et al., 2017).
β-catenin/ZEB1↓,
RadioS↑, Biochanin-A when combined with gamma radiation on HT29 cells, which is resistant to radiation, had revealed a reduction in cell proliferation.
ROS↑, Raised levels of ROS, lipid peroxidation, MMP, caspase-3 have been observed more in the treatment group with significant apoptosis
Casp1↑,
MMP2↓, biochanin-A influenced the tumour invasion capacity by lowering matrix-degrading enzymes (MMP 2 and MMP 9) tested in U87MG cells
MMP9↓,
EGFR↓, Biochanin-A by lowering EGFR, p-ERK (Extracellular signal related kinases), p-AKT (Protein kinase-B), c-myc, and MT-MMP1 (Membrane type matrix metalloproteinase) activation, inhibited cell survival.
ChemoSen↑, Biochanin-A synergistically improved temozolomide anti-cancer ability in GBM
PI3K↓, Cell signalling pathways MAP kinase, PI3 kinase, mTOR, matrix metalloproteases, hypoxia-inducible factor, and VEGF were inhibited by biochanin-A, making it suitable in treating GBM
MMPs↓,
Hif1a↓,
VEGF↓,
*ROS↓, anti-diabetic mechanism of biochanin-A is by decreasing oxidative stress
*Obesity↓, strongly suggest that biochanin-A has therapeutic potential in the treatment of obesity and the prevention of cardiovascular disease
*cardioP↑,
*NRF2↑, Biochanin-A up-regulated the Nrf-2 pathway while suppressing the NF-κB cascade,
*NF-kB↓, By activating the Nrf-2 pathway and inhibiting NF-κB activation, biochanin-A may reduce obesity and its related cardiomyopathy by decreasing oxidative stress and inflammation
*Inflam↓,
*lipid-P↓, cardio-protective effects by controlling lipid peroxidation
*hepatoP↑, biochanin-A influence the elevated hepatic enzyme level, such as AST, ALP, ALT, bilirubin, etc., and found to be a promising molecule in hepatotoxicity models
*AST↓,
*ALP↓,
*Bacteria↓, The results indicate that biochanin-A may be an effective alternate to antibiotics for alleviating SARA in cattles
*neuroP↑, the neuroprotective effects of biochanin-A might be attributed to the activation of the Nrf2 pathway and suppression of the NF-κB pathway
*SOD↑, Biochanin-A reduced oxidative stress in the brain by augmenting SOD (superoxide dismutase) and GSH-Px (glutathione peroxidase) and repressing MDA (malondialdehyde) levels.
*GPx↑,
*AChE↓, Acetylcholinesterase activity was found decreased in a dose-reliant manner amongst biochanin-A treated animals
*BACE↓, Biochanin-A non-competitively inhibited BACE1 with an IC 50 value of 28 μM.
*memory↑, estore learning and memory deficits in ovariectomized (OVX) rats.
*BioAv↓, The bioavailability of biochanin-A is poor.

5638-

BCA,

Investigating the Anticancer Potential of Biochanin A in KB Oral Cancer Cells Through the NFκB Pathway

in-vitro,

Oral,

tumCV↓, BCA treatment induced several notable effects on KB cells, including reduced cell viability, altered morphology suggestive of apoptosis, heightened oxidative stress, and alterations in mitochondrial membrane potential.
ROS↑,
MMP↓,
TumCMig↓, BCA treatment demonstrated an inhibitory effect on cell migration.
TAC↓, revealing decreased antioxidant enzyme activities and increased lipid peroxidation across different BCA concentrations
lipid-P↓,
NF-kB↓, downregulated the expression of nuclear factor-κB (
Apoptosis↑, ts demonstrated ability to induce apoptosis, perturb cellular functions, and modulate gene expression within cancer cells underscores its significance.

6511-

BCP,

Improvement of Oxidative Stress and Mitochondrial Dysfunction by β-Caryophyllene: A Focus on the Nervous System

Review,

AD,

*CB2 / CNR2↑, selective cannabinoid receptor 2 (CB2) agonist
*Bacteria↓, numerous pharmacological activities such as antibacterial (e.g., Helicobacter pylori), antioxidant, anti-inflammatory, analgesic (e.g., neuropathic pain), anti-neurodegenerative and anticancer properties.
*antiOx↑,
*Inflam↓,
*NP/CIPN↓,
*neuroP↑,
AntiCan↑,
*ROS↓, β-caryophyllene in reducing oxidative stress and mitochondrial dysfunction, and its possible links with neuroprotection.
*mtDam↓,
*GSH↑, β-caryophyllene (50 mg/kg/day, i.p. for 4 weeks) ↑ GSH, SOD and CAT. Inhibit lipid peroxidation. ↓ IL-1β, IL-6, and TNF-α levels. ↓ COX-2 and iNOS expression.
*SOD↑,
*Catalase↑,
*lipid-P↓,
*IL1β↓,
*IL6↓,
*TNF-α↓,
*COX2↓,
*iNOS↓,
*NRF2↑, β-caryophyllene (34, 102 and 306 mg/kg/day, p.o.). ↑ Nrf2 and HO-1 expression. Restored SOD and CAT activity and expression.
*HO-1↑,
*AChE↓, Syzygium aromaticum (L.) Merr. and L.M. Perry (0.05 mL/kg and 0.1 mL/kg) ↓ AChE activity, lipid peroxidation levels

6517-

BCP,

β-Caryophyllene Ameliorates Cyclophosphamide Induced Cardiac Injury: The Association of TLR4/NFκB and Nrf2/HO1/NQO1 Pathways

in-vivo,

Nor,

Wistar rats

*cardioP↑, BCP mitigated cardiac markers and lipid peroxidation whereas intensified antioxidant capacity.
*lipid-P↓,
*antiOx↑,
*NRF2↑, BCP activated Nrf2, with subsequent HO1 and NQO1 amplification.
*HO-1↑,
*NQO1↑,
*TLR4↓, inhibited TLR4/NFκB pathways with subsequent enhanced anti-oxidative capacity and diminished inflammatory and apoptosis responses.
*NF-kB↓,
*Inflam↓,
*Apoptosis↓,

6509-

BCP,

βcaryophyllene oxide induces apoptosis and inhibits proliferation of A549 lung cancer cells

in-vitro,

Lung,

A549

tumCV↓, CPO was found to have an inhibitory concentration (IC50) of 124.1 ug/ml.
TumCP↓, Ki67 and PCNA were significantly inhibited after cells were treated with CPO at a concentration of 50 ug/ml compared to controls.
Ki-67↓,
PCNA↓,
P21↓, CPO-treated cells expressed more P21, P53, and DNA strand breaks than controls.
P53↑,
DNAdam↑,
TumCCA↑, accompanied by a significant cell cycle arrest in the S and G2/M phases.
Apoptosis↑, In treated A549 cells, this was also associated with a significant induction of apoptosis, as shown by the upregulation of the expression of caspases 3, 7, and 9, as well as Bax, and the downregulation of Bcl-2.
Casp3↑,
Casp7↑,
Casp9↑,
BAX↑,
Bcl-2↓,
GSH↑, redox status of treated A549 cells revealed a marked rise in GSH and GPx activity levels and a decline in 4-HNE levels, indicating low oxidative stress following CPO treatment of A549 cells.
GPx↑,
4-HNE↑,
ROS↓,
antiOx↑, CPO increased the antioxidants and decreased lipid peroxidation in A549 cells
lipid-P↓,

5561-

betaCar,

Carotenoid Supplementation for Alleviating the Symptoms of Alzheimer’s Disease

Review,

AD,

*ROS↓, Therefore, reducing oxidative stress with antioxidants is a natural strategy to prevent and slow down the progression of AD.
*cognitive↑,
*BBB↑, Carotenoids can cross the blood–brain barrier (BBB) and scavenge free radicals, especially singlet oxygen, which helps prevent the peroxidation of lipids abundant in the brain.
*lipid-P↓,
*eff↑, One of the goals of the food industry should be to encourage the enrichment of food products with functional substances, such as carotenoids, which may reduce the risk of neurodegenerative diseases.

5563-

betaCar,

Carotenoid Supplementation for Alleviating the Symptoms of Alzheimer's Disease

Review,

AD,

*BBB↑, Carotenoids can cross the blood–brain barrier (BBB) and scavenge free radicals, especially singlet oxygen, which helps prevent the peroxidation of lipids abundant in the brain.
*lipid-P↓,
*eff↑, While carotenoids have not been officially approved as an AD therapy, they are indicated in the diet recommended for AD, including the consumption of products rich in carotenoids.
*cognitive↑, A literature review suggests that a diet rich in carotenoids should be promoted to avoid cognitive decline in AD.

5481-

BM,

Therapeutic potential of Bacopa monnieri extracts against hepatocellular carcinoma through in-vitro and computational studies

in-vitro,

HCC,

HepG2

tumCV↓, BME extract showed higher cytotoxicity with less IC50 value (24.70 μg/mL) and a lower percentage of cell viability, while the same extract exhibited 58.65% apoptosis against HepG2 cells in comparison to cisplatin and BMH extract.
Apoptosis↑,
TumCP↓, Different B. monneiri extracts and their valuable phytochemicals showed promising anti-tumor effects by suppressing proliferation, stimulating apoptosis, and reducing migration and invasion in several human cancer cell lines
TumCMig↓,
TumCI↓,
MMP2↓, bacoside A showed an anti-metatastic effect in Wistar albino rats with DEN-induced HCC by downregulating the matrix metalloproteinases (MMP-2 and MMP-9) and lipid peroxidation along with increased antioxidant enzymes levels
MMP9↓,
lipid-P↓,

5473-

BM,

Bacopa monnieri: Preclinical and Clinical Evidence of Neuroactive Effects, Safety of Use and the Search for Improved Bioavailability

in-vivo,

AD,

in-vivo,

Park,

*neuroP↑, results in reducing symptoms and protecting against neurodegeneration.
*toxicity∅, Bacopa monnieri has been found to be generally non-toxic, with no serious side effects reported.
*AChE↓, The neuroprotective effect of Bacopa monnieri was likely due to its ability to inhibit acetylcholinesterase activity rather than mitigating glutamate-induced toxicity.
*ROS↓, neurons treated with the extract exhibited lower levels of reactive oxygen species, suggesting a reduction in intracellular oxidative stress and an extension of neuronal lifespan.
*antiOx↑, The extract also demonstrated antioxidant properties and inhibited lipid peroxidation
*lipid-P↓,
*cognitive↑, on 72 mice, it was shown that supplementation with Bacopa monnieri (100 mg/kg for 180 days) significantly improved cognitive function.
*memory↑, 60 healthy, elderly volunteers taking 300 mg and 600 mg of Brahmi showed reduced acetylcholinesterase activity, which resulted in improved attention and memory.
*Dose↝, Ethanol extract was most commonly used in the studies. Doses are usually in the range of 300 to 600 mg daily.
*BioAv↓, Bacoside A is one of the main active compounds found in Bacopa monnieri. However, its water insolubility results in low bioavailability when administered orally.
*TumCCA↑, It has been shown to induce cell cycle arrest and apoptosis in colorectal cancer cell lines
*BBB↝, Studies were also conducted in which, similarly to the aforementioned approach, formulated solid lipid nanoparticles (SLNs) were used to facilitate the transport of the bacoside-rich extract across the blood–brain barrier.

3698-

BM,

Bacopa monniera prevents from aluminium neurotoxicity in the cerebral cortex of rat brain

in-vivo,

AD,

orally at a dose of 50mg/kg/day

Male Wister rats

*lipid-P↓, Bacopa monniera prevented accumulation of lipid and protein damage significantly, which resulted from aluminium intake.
*ROS↓, Bacopa monniera to inhibit Al-induced oxidative stress was observed
*neuroP↑, Bacopa monniera has potential to protect brain from oxidative damage resulting from aluminium toxicity.

3690-

BM,

Neurocognitive Effect of Nootropic Drug Brahmi (Bacopa monnieri) in Alzheimer's Disease

Review,

AD,

*ROS↓, EBm promotes free radical scavenger mechanisms
*5LO↓, reduces lipoxygenase activity reducing lipid peroxidation, increases glutathione peroxidase and chelates iron.
*lipid-P↓,
*GPx↑,
*IronCh↑,
*neuroP↑, EBm was seen to protect the cholinergic neurons and reduce anticholinesterase activity comparable to donepezil, rivastigmine, and galantamine.
*AChE↓,
*memory↑, EBm improved the total memory score and maximum improvement was seen in logical memory and paired associate learning in humans and reversed phenytoin-induced memory impairment in experimental model.
*toxicity↓, Mild nausea and gastrointestinal upset are seen in humans.
*SOD↑, EBm was administered to the rats for 21 days. It showed increase in activity of enzymes SOD, CAT, and GPx in prefrontal cortex, hippocampus, and striatum. I
*Catalase↑,
*cognitive↑, administration in indicated doses may act as a remedy for age-associated memory and cognitive decline in AD.
*ChAT↑, OBX reduced cholinergic activity and hence also ChAT in hippocampus. Subsequent administration of EBm and tacrine to the substrate, however, reversed this effect
*Ach↑,
*BP↓, Brahmi decreased systolic and diastolic blood pressure without significantly affecting heart rate.

5680-

BML,

Anticancer properties of bromelain: State-of-the-art and recent trends

Review,

Var,

*Inflam↓, anticancer, anti-edema, anti-inflammatory, anti-microbial, anti-coagulant, anti-osteoarthritis, anti-trauma pain, anti-diarrhea, wound repair.
*Bacteria↓,
*Pain↓,
*Diar↓,
*Wound Healing↑,
ERK↓, Figure 1
JNK↓,
XIAP↓,
HSP27↓,
β-catenin/ZEB1↓,
HO-1↓,
lipid-P↓,
ACSL4↑,
ROS↑,
SOD↑,
Catalase↓,
GSH↓,
MDA↓,
Casp3↓,
Casp9↑,
DNAdam↑,
Apoptosis↑,
NF-kB↓,
P53↑,
MAPK↓,
APAF1↑,
Cyt‑c↓,
CD44↓,
Imm↑, Bromelain was also studied in the innate immune system, where it could enhance and sustain the process
ATG5↑,
LC3I↑,
Beclin-1↑,
IL2↓, bromelain in vitro experiments resulted in diminished amounts of IL-2, IL-6, IL-4, G-CSF, Gm-CSF, IFN-γ,
IL4↓,
IFN-γ↓,
COX2↓, proprietary bromelain extract could decrease IL-8, COX-2, iNOS, and TNF-α without affecting cell viability.
iNOS↓,
ChemoSen↑, Bromelain may increase the cytotoxicity of cisplatin in the treatment of breast cancer as reported in 2 studies with MDA-MB-231 and 4T1 Breast Tumor cell lines
RadioS↑, The size and weight of tumors in gamma-irradiated EST-bearing mice treated with bromelain decreased significantly with a significant amelioration in the histopathological examination
Dose↝, oral bromelain administration in breast cancer patients (daily up to a dose of 7800 mg)
other↓, The role of bromelain (in combination with papain, sodium selenite and Lens culinaris lectin) has been also tested as a complementary medicine on more than 600 breast cancer patients to reduce the side effects caused by the administration of the adju

3516-

Bor,

Boron in wound healing: a comprehensive investigation of its diverse mechanisms

Review,

Wounds,

*Inflam↓, anti-inflammatory, antimicrobial, antioxidant, and pro-proliferative effects.
*antiOx↑,
*ROS↓, The antioxidant properties of boron help protect cells from oxidative stress, a common feature of chronic wounds that can impair healing
*angioG↑, Boron compounds exhibit diverse therapeutic actions in wound healing, including antimicrobial effects, inflammation modulation, oxidative stress reduction, angiogenesis induction, and anti-fibrotic properties.
*COL1↑, Boron has been shown to increase the expression of proteins involved in wound contraction and matrix remodeling, such as collagen, alpha-smooth muscle actin, and transforming growth factor-beta1.
*α-SMA↑,
*TGF-β↑,
*BMD↑, Animals treated with boron showed favorable changes in bone density, wound healing, embryonic development, and liver metabolism
*hepatoP↑,
*TNF-α↑, BA elevates TNF-α and heat-shock proteins 70 that are related to wound healing.
*HSP70/HSPA5↑,
*SOD↑, antioxidant properties of BA showed that boron protects renal tissue from I/R injury via increasing SOD, CAT, and GSH and decreasing MDA and total oxidant status (TOS)
*Catalase↑,
*GSH↑,
*MDA↓,
*TOS↓,
*IL6↓, Boron supports gastric tissue by alleviating ROS, MDA, IL-6, TNF-α, and JAK2/STAT3 action, as well as improving AMPK activity
*JAK2↓,
*STAT3↓,
*AMPK↑,
*lipid-P↓, boron may improve wound healing by hindering lipid peroxidation and increasing the level of VEGF
*VEGF↑,
*Half-Life↝, Boron is a trace element, usually found at a concentration of 0–0.2 mg/dL in plasma with a half-life of 5–10 h, and 1–2 mg of it is needed in the daily diet

3510-

Bor,

Boron Affects the Development of the Kidney Through Modulation of Apoptosis, Antioxidant Capacity, and Nrf2 Pathway in the African Ostrich Chicks

in-vivo,

Nor,

ostrich chicks

*RenoP↑, Our results revealed that low doses of boron (up to 160 mg) had positive effect, while high doses (especially 640 mg) caused negative effect on the development of the kidney
*ROS↓, The low doses regulate the oxidative and enzyme activity in the kidney.
*antiOx↑, boron at low doses upregulated the expression of genes involved in the antioxidant pathway
*Apoptosis↓, low levels of boron (up to 160 mg) inhibited the cell apoptosis, regulate the enzyme activity, and improved the antioxidant system, thus may encourage the development of the ostrich chick's kidney
*NRF2↑, maximum localization of Nrf2 in 80 mg/L BA dose group
*HO-1↑, As the boron concentration increased, the expression of Nrf2, GCLc, and HO-1 genes upregulated
*MDA↓, In comparison to those of the group 1, MDA content (lipid peroxidation marker) was significantly decreased by 26.02 and 48.12% in the 40 and 80 mg/L BA groups
*lipid-P↓,
*GPx↓, GSH-PX activity of ostrich chick kidney tissue was slightly increased in the 40 and 80 mg/L BA groups,
*Catalase↑, supplementation of low doses of boron in the ostrich drinking water has resulted in stimulation of antioxidant capacity of GR, CAT, and SOD significantly.
*SOD↑,
*ALAT↓, boron supply in low doses (especially 80 mg/L BA) showed decrease levels in the activity of ALT, AST, and ALP.
*AST↓,
*ALP↓,

760-

Bor,

Therapeutic Efficacy of Boric Acid Treatment on Brain Tissue and Cognitive Functions in Rats with Experimental Alzheimer’s Disease

in-vivo,

AD,

rats

*memory↑, BA reduced damage to learning and memory functions and significantly lowered oxidative stress markers in the AD model.
*ROS↓, been reported that BA also reduces oxidative stress by increasing glutathione reserves,
*GSH↑,
*Aβ↓, and strongly inhibits Aβ aggregation via hydroxyl group
*Inflam↓, BA can act as a protective agent in apoptotic processes by regulating oxidative and inflammatory processes as well as mitochondrial membrane potential
*MMP↑,
*lipid-P↓, BA added to the diet prevented lipid peroxidation by supporting and strengthening the antioxidant defense system.
*Ca+2↓, Boron is thought to prevent apoptosis and strengthen antioxidant defense by reducing intracellular oxygen radicals and calcium levels.
*cognitive↑, Our hypothesis is that boric acid can improve cognitive function and histopathological outcomes by reducing oxidative stress in rats with STZ-induced Alzheimer’s Disease
*TOS↓, After BA administration, it increased TAS by increasing the antioxidant effect, and as a result, TOS and OSI decreased.

4270-

Bos,

Boswellic acids ameliorate neurodegeneration induced by AlCl3: the implication of Wnt/β-catenin pathway

in-vivo,

AD,

 6 weeks, rats were treated daily with AlCl3

*memory↑, BA significantly improved learning and memory impairments induced by AlCl3 treatment.
*AChE↓, BA treatment significantly decreased acetylcholinesterase levels and reduced amyloid-beta (Aβ) expression
*Aβ↓,
*TNF-α↓, BA ameliorated the increased expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), inhibited lipid peroxidation, and increased total antioxidants in the brain.
*IL1β↓,
*lipid-P↓,
*TAC↑,
*BDNF↑, Indeed, BA significantly suppressed AlCl3-induced decrease of brain-derived neurotrophic factor, pGSK-3β (Ser 9), and β-catenin.
*β-catenin/ZEB1↑,
*Dose↑, BA (250 mg/kg) showed a significant protective effect compared to a lower dose.

1425-

Bos,

Protective Effect of Boswellic Acids against Doxorubicin-Induced Hepatotoxicity: Impact on Nrf2/HO-1 Defense Pathway

in-vivo,

Nor,

*ChemoSen↑, BAs significantly improved the altered liver enzyme activities and oxidative stress markers.
*NRF2↑, BAs increased the Nrf2 and HO-1 expression, which provided protection against DOX-induced oxidative insult
*HO-1↑,
*ROS↓, appear to scavenge ROS and inhibit lipid peroxidation and DNA damage of DOX-induced hepatotoxicity
*lipid-P↓,
*DNAdam↓,

5713-

Brut,

Standardized bergamot polyphenolic fraction – a comprehensive dietary supplement with pleiotropic properties compared to other selected natural lipid-lowering substances available on the market

Review,

Nor,

*eff↑, Standardized bergamot polyphenolic fraction has the same polyphenol profile as in the juice, but flavonoids are over 200 times more concentrated.
*lipid-P↓,

6542-

BSB,

Health Benefits, Pharmacological Effects, Molecular Mechanisms, and Therapeutic Potential of α-Bisabolol

Review,

Var,

Review,

Park,

Review,

AD,

AntiCan↑, Numerous experimental studies demonstrated pharmacological properties of α-Bisabolol including anticancer, antinociceptive, neuroprotective, cardioprotective, and antimicrobial.
*neuroP↑,
*cardioP↑,
*AntiBio↑,
*BioAv↑, Given the polypharmacological effects and pleiotropic properties, along with favorable pharmacokinetics, and dietary availability and safety, α-Bisabolol can be used as a dietary agent, nutraceutical or phytopharmaceutical agent or as an adjuvant wit
*toxicity↓,
*BioAv↑, integrated in many cosmetic formulations due to its skin soothing effects, well documented dermal absorption
*motorD↑, improvement in locomotor activity, a reduction in the expression of thiol and a reinstate of the activity of mitochondrial complex-I.
*SOD↑, α-Bisabolol also increased the mRNA level of antioxidants proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product.
*Catalase↑,
*Keap1↑,
*MDA↓, α-Bisabolol attenuated oxidative insult by reducing malondialdehyde (MDA), restoring depleted glutathione (GSH) and improving SOD and CAT activity.
*GSH↑,
*IL1β↓, attenuated neuroinflammation by reducing glial cells activation and subsequent release of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and mediators (iNOS and COX-2).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2↓,
*lipid-P↓, α-Bisabolol restored mitochondrial function by preventing mitochondrial lipid peroxidation, cytochrome-C release and most importantly preserving Complex-I activity
*Cyt‑c↓,
*ROS↓, The study concluded that α-Bisabolol safeguarded against the induced upsurge of ROS and nitrite.
*MMP↑, α-Bisabolol treatment also restored mitochondrial membrane potential (MMP) validating its antioxidant effect.
*antiOx↑,
*AChE↓, showed a significant reduction in AChE activity and an ability to avert Ach depletion.
*Apoptosis↓, α-Bisabolol protected cells from Aβ triggered apoptosis by reducing Bax and Caspase-3 and increasing Bcl-2 activity.
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BACE↓, α-Bisabolol inhibitory activity on BACE1 and found a decrease in BACE1 activity following α-Bisabolol treatment
*BChE↓, AChE, BuChE, β-secretase actions were decreased significantly in cells pretreated with α-Bisabolol
*eff↑, The compound clearly illustrated a potent anti-AchE activity of 95.869% similar to the activity of donepezil, a standard drug. I
*Aβ↓, The compound also disaggregated Aβ25–35 peptide and protected against its induced toxicity by increasing neuro2a cells viability [
*ATP↑, figure 2
RadioS↑, α-Bisabolol and Anticancer Effects, figure 3
Cyt‑c↑,
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↑,
PARP↑,
BAX↑,
BID↑,
NF-kB↑,
Fas↑,
EGFR↑,
TIMP2↑,
XIAP↓,
COX2↓,
Bak↓,
Bcl-2↓,
P53↑, The expression of p53 (a transcription factors whose products might lead to apoptosis), NF-κB and Fas was increased following α-Bisabolol treatment, indicating their function in mediating α-Bisabolol-induced apoptosis in the cancer cell line.
HER2/EBBR2↓,
FGF↓,
CEA↓,
Akt↓,
TumCCA↑, α-Bisabolol suppresses the cellular proliferation at G2/M cell cycle phase.
*Imm↑, reported that α-Bisabolol boosted the immunity response by T-cell subsets (CD4 and CD8) supplementation in treated mice.
*CD4+↑,
*CD8+↑,
*BBB↑, ↑ BBB penetration
*Pain↓, α-Bisabolol based mouthwash to that of chlorhexidine in reducing pain during brushing
*cardioP↑, α-Bisabolol and Cardioprotection, figure 5
*TBARS↓, rats co-treated with α-Bisabolol showed reduced LOOH and TBARS and increased SOD, CAT and GSH.
*SOD↑,
*Catalase↑,
*GSH↑,
*AntiBio↑, α-Bisabolol demonstrated an antibacterial effect against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa as well as a synergism against S. aureus, when combined with the antibiotic norfloxacin and against E. coli when combined with
*AntiFungal↑, ↓ fungal growth
*GastroP↑, α-Bisabolol and Gastroprotection. oral administration of α-Bisabolol was realized to attenuate gastric damage and to provide cytoprotection in stomach.
*RenoP↑, The nephroprotective effects of α-Bisabolol and the underlying mechanisms are summarized in Table 10.
*creat↓, ↓ creatinine, urea, uric acid
*uricA↓,
*Inflam↓, Anti-Inflammatory Effects of α-Bisabolol
*iNOS↓, ↓ iNOS, COX-2, TNF-α, p65 PGE2, nitrite, IL-6, ↓ MMP13
*COX2↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,

6554-

BSB,

doxoR,

α-Bisabolol: A Dietary Sesquiterpene that Attenuates Apoptotic and Nonapoptotic Cell Death Pathways by Regulating the Mitochondrial Biogenesis and Endoplasmic Reticulum Stress–Hippo Signaling Axis in Doxorubicin-Induced Acute Cardiotoxicity in Rats

in-vivo,

Nor,

 25 mg/kg of BSB orally twice a day.

rats

*cardioP↑, results that are currently available unequivocally show the cardioprotective role of BSB in DOX-induced cardiotoxicity.
*chemoP↑, BSB preserves the myocardium and reverses all cellular, molecular, and structural disruptions in the cardiac tissues of rats exposed to DOX-induced toxicity.
*antiOx↑, effect is attributed to BSB’s strong antioxidant, antilipid peroxidative, and antiapoptotic properties
*ROS↓,
*toxicity↓, BSB has been listed by the United States Food and Drug Administration (US FDA) as “generally regarded as safe” (GRAS) owing to its low toxicity.
*DNAdam↓, BSB Prevents DOX-Induced DNA Damage
*lipid-P↓, BSB Inhibits Lipid Peroxidation and Improves Antioxidants, ETC Complex, and TCA Cycle Enzymes
*ER Stress↓, BSB suppressed ER-stress-mediated myocardial Hippo-YAP activation and necroptosis against DOX-induced cardiotoxicity.

Showing Research Papers: 1 to 50 of 224
Page 1 of 5 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 224

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiBio↑, 3, TRPA1↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1, antiOx↑, 24, Catalase↑, 12, Ferroptosis↓, 3, GPx↓, 1, GPx↑, 7, GPx4∅, 1, GSH↑, 17, GSR↑, 2, GSTs↓, 1, GSTs↑, 3, H2O2↓, 1, HO-1↑, 6, HO-1∅, 1, Keap1↓, 1, Keap1↑, 1, lipid-P↓, 43, MDA↓, 7, MPO↓, 1, NQO1↑, 3, NRF2↑, 9, NRF2∅, 1, RNS↓, 1, ROS↓, 30, ROS↑, 1, SOD↑, 15, TAC↑, 2, TBARS↓, 2, TOS↓, 2, uricA↓, 1, VitC↑, 2, VitE↑, 2,

Metal & Cofactor Biology(tgid=2) ⓘ

FTH1↑, 1, IronCh↑, 6, TfR1/CD71↓, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 2, ATP∅, 1, MMP↓, 1, MMP↑, 2, mtDam↓, 2,

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↑, 1, Acetyl-CoA↑, 3, ACSL4∅, 1, adiP↑, 1, ALAT↓, 3, AMPK↑, 1, p‑AMPK↑, 1, GlucoseCon↑, 5, H2S↑, 1, LDH↓, 3, LDL↓, 1, NADPH↑, 2, PPARγ↓, 1,

Cell Death(tgid=5) ⓘ

Akt↓, 2, Apoptosis↓, 6, BAX↓, 3, Bcl-2↑, 1, Casp3↓, 1, cl‑Casp3↓, 1, Cyt‑c↓, 2, Fas↓, 1, Ferroptosis↓, 3, iNOS↓, 6, JNK↓, 1, MAPK↓, 2, p38↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 5, other↓, 2, other↑, 1, other↝, 1,

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1, HSP70/HSPA5↑, 1,

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1, LC3B↑, 1, p62↓, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 4, DNArepair↑, 1,

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1, GSK‐3β↓, 2, IGF-1↑, 1, PI3K↓, 2, STAT3↓, 1,

Migration(tgid=13) ⓘ

5LO↓, 2, APP↓, 1, Ca+2↓, 2, Ca+2↝, 1, CD31↑, 1, COL1↑, 1, MMP13↓, 1, N-cadherin↑, 1, TGF-β↑, 1, VCAM-1↓, 2, ZO-1↑, 1, α-SMA↑, 1, β-catenin/ZEB1↑, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 2, NO↓, 4, VEGF↑, 2,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 10, BBB↝, 1, GastroP↑, 1, GLUT3↑, 1, GLUT4↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

CB2 / CNR2↑, 1, CD4+↑, 1, COX2↓, 6, CRP↓, 1, ICAM-1↓, 1, IFN-γ↓, 1, IL10↑, 1, IL1β↓, 10, IL4↓, 1, IL6↓, 9, IL6↑, 1, IL8↓, 1, Imm↑, 2, Inflam↓, 23, JAK2↓, 1, MCP1↓, 1, MUC2↓, 1, NF-kB↓, 11, PGE2↓, 5, TLR4↓, 1, TNF-α↓, 11, TNF-α↑, 1,

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 2, AChE↓, 12, BChE↓, 3, BDNF↑, 2, ChAT↑, 6, MAOA↓, 2, tau↓, 2, p‑tau↓, 3,

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1, Aβ↓, 11, BACE↓, 4, MAOB↓, 3, NLRP3↓, 1,

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CYP19↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 3, BioAv↑, 10, BioAv↝, 2, ChemoSen↑, 2, Dose↑, 1, Dose↝, 3, eff↑, 8, Half-Life↓, 2, Half-Life↝, 4,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 3, ALP↓, 2, AST↓, 4, BMD↑, 1, BP↓, 2, creat↓, 2, CRP↓, 1, GutMicro↑, 2, IL6↓, 9, IL6↑, 1, LDH↓, 3, MUC19↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1, AntiCan↑, 2, AntiDiabetic↓, 1, AntiDiabetic↑, 2, cardioP↑, 12, chemoP↑, 1, cognitive↑, 16, cognitive∅, 2, hepatoP↑, 5, memory↑, 16, motorD↑, 2, neuroP↑, 24, NP/CIPN↓, 1, Obesity↓, 1, Pain↓, 2, RenoP↑, 4, Sleep↑, 1, Strength↑, 1, toxicity↓, 6, toxicity∅, 2, Weight↓, 1, Wound Healing↑, 2,

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 3, AntiViral↑, 2, Bacteria↓, 4, CD8+↑, 1, Diar↓, 1,
Total Targets: 190

Scientific Paper Hit Count for: lipid-P, lipid peroxidation

13 Curcumin
13 Quercetin
13 Thymoquinone
11 Silymarin (Milk Thistle) silibinin
9 Alpha-Lipoic-Acid
9 Resveratrol
7 Eugenol
7 Rosmarinic acid
7 Urolithin
6 Berberine
6 Carvacrol
6 Crocetin
6 Lycopene
5 Luteolin
5 Cinnamon
4 Ashwagandha(Withaferin A)
4 Bacopa monnieri
4 Centella asiatica / Gotu kola → asiaticoside
4 Chrysin
4 Selenium NanoParticles
3 Allicin (mainly Garlic)
3 Beta-Caryophyllene
3 Boron
3 α-Bisabolol / Chamomile oil
3 Chemotherapy
3 Dandelion Root
3 EGCG (Epigallocatechin Gallate)
3 Ferulic acid
3 Moringa oleifera
3 Pterostilbene
2 1,8-Cineole
2 Astaxanthin
2 Baicalein
2 Biochanin A
2 beta-carotene(VitA)
2 Boswellia (frankincense)
2 doxorubicin
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Propolis -bee glue
2 Carnosine
2 chitosan
2 Coenzyme Q10
2 Selenium
2 Vitamin E
2 Fisetin
2 Shilajit/Fulvic Acid
2 Graviola
2 Hydrogen Gas
2 Piperine
2 Rutin
2 Radiotherapy/Radiation
1 Atorvastatin
1 Aloe anthraquinones
1 Bromelain
1 Bruteridin(bergamot juice)
1 Caffeic acid
1 Capsaicin
1 Thymol-Thymus vulgaris
1 Chlorogenic acid
1 Chlorophyllin
1 Vitamin C (Ascorbic Acid)
1 Chocolate
1 Cichoric acid / Chicoric acid
1 methotrexate
1 Carica papaya leaf extract
1 Copper and Cu NanoParticles
1 diet Fermented Foods
1 D-limonene
1 Cisplatin
1 Emodin
1 Hydroxycinnamic-acid
1 Melatonin
1 Naringin
1 Nimbolide
1 Phenethyl isothiocyanate
1 Piperlongumine
1 Phosphatidylserine
1 Silver-NanoParticles
1 Shankhpushpi
1 Selenite (Sodium)
1 Taurine
1 5-fluorouracil
1 Turmerones
1 Vitamin B5,Pantothenic Acid

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:453  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

lipid-P Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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