antiOx Cancer Research Results

antiOx, anti-oxidant activities: Click to Expand ⟱

Source:

Type:

Various antioxidants such as Nrf2, SODs, catalase, GPxs, PRDXs, and GSTs are altered in different cancers and have been linked to prognosis. Their overexpression can correlate with aggressive tumor behavior and resistance to treatment in many contexts.

Scientific Papers found: Click to Expand⟱

3971-

ACNs,

Blueberry Supplementation Improves Memory in Older Adults

Human,

AD,

wild blueberry juice in a sample of nine older adults with early memory changes

*antiOx↑, Blueberries contain polyphenolic compounds, most prominently anthocyanins, which have antioxidant and anti-inflammatory effects.
*Inflam↓,
*memory↑, anthocyanins have been associated with increased neuronal signaling in brain centers mediating memory function as well as improved glucose disposal, benefits that would be expected to mitigate neurodegeneration.
*neuroP↑, preliminary study suggest that moderate-term blueberry supplementation can confer neurocognitive benefit
*cognitive↑, At 12 weeks, we observed improved paired associate learning (p = 0.009) and word list recall (p = 0.04).
*Mood↑, In addition, there were trends suggesting reduced depressive symptoms (p = 0.08) and lower glucose levels (p = 0.10)
*glucose↓,

3864-

ACNs,

Anthocyanins Potentially Contribute to Defense against Alzheimer’s Disease

Review,

AD,

*antiOx↑, ANTs are potent antioxidants that might regulate the free radical-mediated generation of amyloid peptides (Abeta-amyloids) in the brain
*Aβ↓,
*ROS↓,
*cognitive↑, Mulberries are a rich source of ANTs that induce antioxidant enzymes and promote cognition
*APP↓, In the cerebral cortex, blackcurrant and bilberry extract reduced APP levels in AD mouse models, but changes in the expression or phosphorylation of tau-protein were not observed
*BBB↑, ANTs cross the blood-brain barrier and protect brain tissue from Abeta toxicity
*Ca+2↓, Aronia melanocarpa. ANTs of this plant decrease intracellular calcium and ROS but increase ATP and mitochondrial potential.
*ATP↑,
*BACE↓, An-NPs also attenuate the protein expression of BACE-1 neuroinflammatory markers, such as phosphonuclear factor kB (p-NF-kB), tumor-necrosis factor (TNF-α), and inducible nitric oxide synthase (iNOS),
*p‑NF-kB↓,
*TNF-α↓,
*iNOS↓,

5444-

AG,

A Systematic Review of Phytochemistry, Pharmacology and Pharmacokinetics on Astragali Radix: Implications for Astragali Radix as a Personalized Medicine

Review,

Var,

*Imm↑, AR possesses various biological functions, including potent immunomodulation, antioxidant, anti-inflammation and antitumor activities.
*antiOx↑,
*Inflam↓,
AntiTum↑,
eff↑, characteristics of increasing curative effect and reducing the toxicity of chemotherapeutic drugs [11 , 118].
chemoP↑,
Dose↝, main bioactive compounds responsible for the anti-cancer effects of AR mainly include formononetin, AS-IV and APS. S
TumCMig↓, AS-IV could inhibit the migration and proliferation of non-small cell lung cancer (NSCLC
TumCP↓,
Akt↓, h via inhibition of the Akt/GSK-3β/β-catenin signaling axis.
GSK‐3β↓,
MMP2↓, downregulating the expression of matrix metalloproteases (MMP)-2 and -9
MMP9↓,
EMT↓, AS-IV could inhibit TGF-B1 induced EMT through inhibition of PI3K/AKT/NF-KB
PI3K↓,
Akt↓,
NF-kB↓,
Inflam↓,
TGF-β1↓,
TNF-α↓,
IL6↓,
Fas↓, reduced FAS/FasL
FasL↓,
NOTCH1↓, decressing notch1
JNK↓, inactivating JNK pathway [145]
TumCG↓, The results showed that the AR water extract could inhibit the growth of colorectal cancer in vivo without apparent toxicity and side effect, which suggests that AR is a potential therapeutic drug for colorectal cancer

1594-

AgNPs,

Citrate,

Silver Citrate Nanoparticles Inhibit PMA-Induced TNFα Expression via Deactivation of NF-κB Activity in Human Cancer Cell-Lines, MCF-7

in-vitro,

BC,

MCF-7

TNF-α↓, AgNPs-CIT inhibited TNFα expression via deactivation of the NF-κB signaling event
NF-kB↓,
antiOx↑, best antioxidant activity of AgNPs-CIT was found at >40% (~ 42%) radicals inhibitions at 10 mg/mL concentration
TumCP↓, cancer cell proliferation was significantly decreased when pretreated with AgNPs-CIT for 2 h and then stimulated with PMA for 24 h

4397-

AgNPs,

Synthesis and Characterization of Silver Nanoparticles from Rhizophora apiculata and Studies on Their Wound Healing, Antioxidant, Anti-Inflammatory, and Cytotoxic Activity

NA,

Wounds,

 99 nm, with a zeta potential of −6 mV

selectivity↑, The cytotoxicity cell viability assay revealed that the AgNPs were less toxic (IC50 105.5 µg/mL) compared to the R. apiculata extract (IC50 47.47 µg/mL) against the non-cancerous fibroblast L929 cell line.
tumCV↓, AgNPs showed considerable cytotoxic effect, and the percentage of cell viability against skin cancer, lung cancer, and oral cancer cell lines was 31.84%, 56.09% and 22.59%, respectively.
antiOx↑, AgNPs exhibited potential antioxidant, anti-inflammatory, wound healing, and cytotoxic properties
Inflam↓,

4392-

AgNPs,

Hepatocurative activity of biosynthesized silver nanoparticles fabricated using Andrographis paniculata

in-vivo,

LiverDam,

13-27 nm. Zeta potential was -34.3 mV indicating stable AgNPs.

 CCl(4) induced liver injury.

*antiOx↑, strong antioxidant effect of the AgNPs compared to 5% aqueous leaf extract.
*eff?, effective in revival of all biological parameters to near normal in all intoxicated groups indicating the curing effects on CCl(4) induced liver injury.

4412-

AgNPs,

Biosynthesis and characterization of silver nanoparticles from Asplenium dalhousiae and their potential biological properties

in-vitro,

CRC,

HCT116

in-vitro,

Melanoma,

A2780S

Bacteria↓, The antioxidant activity of the synthesized AgNPs was assessed using the DPPH method, which confirmed their significant antioxidant properties alongside their antibacterial activity.
antiOx↑, AgNPs but also exhibits substantial antioxidant properties
AntiCan↑, anticancer activities
eff↑, The combination of Asplenium dalhousiae leaf methanolic extracts and synthesized silver nanoparticles (AgNPs: aqueous, n-hexane, and CHCl3 fractions) exhibits varied apoptotic activity against ovarian and colorectal cancer cells.

4407-

AgNPs,

Green Synthesis and Characterization of Silver Nanoparticles from Eclipta alba and Its Activity Against Triple-Negative Breast Cancer Cell Line (MDA-MB-231)

in-vitro,

BC,

MDA-MB-231

 40-60 nm

antiOx↑, Further in vitro anti-oxidant analysis results revealed that green synthesized AgNPs showed 2.6-fold higher anti-oxidant potential (IC50 15.70 g/ml) than that of aqueous plant leaf extract (IC50 39.80 g/ml).
TumCG↓, Eclipta alba leaf extract actively bonded with silver nanoparticles suppresses the MDA-MB-231 cells growth through high antioxidant characters and anti-leishmanial activity.

4364-

AgNPs,

Selective cytotoxicity of green synthesized silver nanoparticles against the MCF-7 tumor cell line and their enhanced antioxidant and antimicrobial properties

in-vitro,

BC,

MCF-7

31.4 nm with a Zeta potential of −33.8 mV,

TumCD↑, AgNPs and the extract exhibited 70% and 40% cytotoxicity against MCF-7 cancerous cells, respectively, while CSN caused 56% cell death (at the concentration of 60 µg/mL)
selectivity↑, It was observed that AgNPs were much less cytotoxic when tested against a noncancerous cell line (L-929)
*antiOx↑, These include antioxidant, antifungal, anti-inflammatory, antiviral, anti-angiogenesis, and antimicrobial effects
*Inflam↓,
AntiTum↑, antitumor properties of AgNPs
ROS↑, AgNPs interact with mitochondria and disrupt the cellular electron transfer chain function leading to an increase in the ROS level. oxidative stress generated by ROS could be considered as a main toxicity mechanism of AgNPs against cells

4560-

AgNPs,

Exploiting antidiabetic activity of silver nanoparticles synthesized using Punica granatum leaves and anticancer potential against human liver cancer cells (HepG2)

in-vitro,

Liver,

HepG2

in-vitro,

Diabetic,

AntiCan↑, The PGE-AgNPs showed a dose-dependent response against human liver cancer cells (HepG2) (IC50; 70 μg/mL) indicating its greater efficacy in killing cancer cells.
Dose↝, surface charge of synthesized AgNPs was highly negative (−26.6 mV) and particle size distribution was ranging from ∼35 to 60 nm and the average particle size was about 48 nm determined by dynamic light scattering (DLS)
*antiOx↑, literature suggests that AgNPs display considerable antioxidant activity in vitro
*AntiDiabetic↑, Antidiabetic potential of biosynthesized AgNPs
*Bacteria↓, Synergistic antibacterial potential of AgNPs with standard antibiotics

4541-

AgNPs,

RosA,

Eco-friendly synthesis of silver nanoparticles: multifaceted antioxidant, antidiabetic, anticancer, and antimicrobial activities

in-vitro,

Nor,

WI38

in-vitro,

BC,

MDA-MB-231

in-vitro,

PC,

PANC1

*antiOx↑, Potent antioxidant activity was observed with an EC₅₀ of 7.81 µg mL⁻1, close to ascorbic acid (3.27 µg mL⁻1).
TumCD↓, Ag-NPs showed selective cytotoxicity against MDA and PANC-1 cells (IC₅₀: 177.2 and 115.3 µg mL⁻1), with lower toxicity toward Vero and Wi38 normal cells (IC₅₀: 233 and 207 µg mL⁻1).
selectivity↑,

2206-

AgNPs,

RES,

ENHANCED EFFICACY OF RESVERATROL-LOADED SILVER NANOPARTICLE IN ATTENUATING SEPSIS-INDUCED ACUTE LIVER INJURY: MODULATION OF INFLAMMATION, OXIDATIVE STRESS, AND SIRT1 ACTIVATION

in-vivo,

Nor,

Rats

*hepatoP↑, AgNPs + RV treatment significantly reduced pro-inflammatory cytokines, NF-κB activation, presepsin, PCT, 8-OHDG, and VEGF levels compared with the CLP group, indicating attenuation of sepsis-induced liver injury.
*Inflam↓,
*NF-kB↓,
*VEGF↓,
*SIRT1↑, Both RV and AgNPs + RV treatments increased SIRT1 levels, suggesting a potential role of SIRT1 activation in mediating the protective effects.
*ROS↓, alleviating sepsis-induced liver injury by modulating inflammation, oxidative stress, and endothelial dysfunction, potentially mediated through SIRT1 activation.
*Dose↝, 30 mg/kg of AgNPs + RV was given intraperitoneally to the rats
*Catalase↑, AgNPs + RV treatment exhibited a robust effect in bolstering CAT activity
*MDA↓, AgNPs + RV treatment effectively ameliorates sepsis-induced oxidative stress and inflammation in rat livers by reducing MDA, MPO, and NO levels
*MPO↓,
*NO↓,
*ALAT↓, AgNPs + RV effectively reduced the ALT and AST levels, returning them to values similar to those observed in the Sham group
*AST↓,
*antiOx↑, corroborates the antioxidant potential of RV and AgNPs observed in earlier studies

2205-

AgNPs,

Potential protective efficacy of biogenic silver nanoparticles synthesised from earthworm extract in a septic mice model

in-vivo,

Nor,

mice, septic

*Dose↝, The treated group received a single oral dose of 5.5 mg/kg of Ag NPs. 5 to 12 nm
*eff↑, Ag NPs treatment in septic mice significantly decreased liver enzyme activities, total protein, and serum albumin.
*RenoP↑, Ag NPs significantly enhanced kidney function, as indicated by a significant decrease in the levels of creatinine, urea, and uric acid.
*antiOx↑, Ag NPs showed a powerful antioxidant effect via the considerable reduction of malondialdehyde and nitric oxide levels and the increase in antioxidant content.
*MDA↓,
*NO↓,
*hepatoP↑, hepatoprotective effect of Ag NPs may be attributed to their antioxidant properties
*toxicity↝, The Ag NPs dose is 1/10 of LD50, which is 5.5 mg/kg.
*GSH↑, GSH, SOD, GST, and CAT of the septic group. Meanwhile, the Ag NPs-treated mice showed a significant (p < 0.05) increase in all four parameters.
*SOD↑,
*GSTs↑,
*Catalase↑,

5344-

Ajoene,

Ajoene, a Stable Garlic By-Product, Has an Antioxidant Effect through Nrf2-Mediated Glutamate-Cysteine Ligase Induction in HepG2 Cells and Primary Hepatocytes

in-vitro,

Nor,

HepG2

*Nrf1↑, Ajoene treatment activated Nrf2, as indicated by increased phosphorylation and nuclear accumulation of Nrf2
*PKCδ↑, Ajoene activated protein kinase C-δ (PKCδ).
*GSH↑, Our results demonstrate that ajoene increases PKCd-dependent Nrf2 activation, GCL induction, and the cellular GSH concentration, which may contribute to protecting cells from oxidative stress.
*antiOx↑,

5354-

AL,

Therapeutic Potential of Allicin-Rich Garlic Preparations: Emphasis on Clinical Evidence toward Upcoming Drugs Formulation

Review,

Var,

*LDL↓, Indeed, clinical studies on healthy subjects have evidenced that standardized garlic treatment (900 mg/day) significantly reduces total cholesterol (TC) and low-density lipoprotein cholesterol (c-LDL).
*antiOx↑, Multiple studies have focused on allicin therapeutic potential as an antioxidant (inducing antioxidant product production),
AntiCan↑, anticancer (triggering cancer cells apoptosis and inhibiting tumor growth),
*cardioP↑, cardioprotective (decreasing angiogenesis and inducing vasorelaxation)
*BP↓, Conversely, aged garlic extract supplementation was shown to be more effective than the placebo in lowering systolic blood pressure
*Weight↓, Garlic powder supplementation (800 mg/daily) resulted in a significant decrease in body weight and body fat mass (
NK cell↑, Actually, aged garlic administration in patients with advanced cancer of the digestive system led to an improvement of natural killer (NK) cell activity but did not cause improvement in QoL
*AntiDiabetic↑, Actually, daily garlic allicin supplementation (0.05–1.5 g) displayed a positive and sustained role in blood glucose, total cholesterol (TC), and high/low density lipoprotein (HDL-c/LDL-c) regulation in type 2 diabetes mellitus (T2DM) management
*GSH↑, 2-month application of coated garlic powder tablets (900 mg with alliin and allicin contents of 1.3% and 0.6%, respectively), the glutathione (GSH) concentration significantly increased in circulating human erythrocytes

2558-

AL,

Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment

Review,

AD,

*AntiCan↑, Allicin has shown anticancer, antimicrobial, antioxidant properties and also serves as an efficient therapeutic agent against cardiovascular diseases
*antiOx↑,
*cardioP↑,
*neuroP↑, present review describes allicin as an antioxidant, and neuroprotective molecule
cognitive↑, that can ameliorate the cognitive abilities in case of neurodegenerative and neuropsychological disorders.
*ROS↓, As an antioxidant, allicin fights the reactive oxygen species (ROS) by downregulation of NOX (NADPH oxidizing) enzymes, it can directly interact to reduce the cellular levels of different types of ROS produced by a variety of peroxidases.
*NOX↓,
*TLR4↓, inhibition of TLR4/MyD88/NF-κB, P38 and JNK pathways.
*NF-kB↓,
*JNK↓,
*AntiAg↑, A low concentration of allicin (0.4 mM) can inhibit the platelet aggregation up to 90%, the impact is significantly higher than of similar concentration of aspirin.
*H2S↑, Allicin decomposes rapidly and undergoes a series of reactions with glutathione resulting in the production of hydrogen sulphide (H2S).
*BP↓, H2S is a gaseous signalling molecule involved in the regulation of blood pressure.
Telomerase↓, Allicin inhibits the activity of telomerase in a dose dependent manner subsequently inhibiting the proliferation in the cancer cells
*Insulin↑, Studies have shown a significant increase in the blood insulin levels after treatment with allicin
BioAv↝, optimum temperature for the activity of alliinase is 33 °C, it operates best at pH 6.5, the enzyme is sensitive to acids [42,43] (Figure 3), enteric-coated formulations of garlic supplements are therefore recommended
*GSH↑, It helps to lower the hyperglycaemic conditions and improves the glutathione and catalase biosynthesis [37,38]
*Catalase↑,

2770-

AL,

Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis

in-vivo,

Nor,

 50 mg /kg

Male Sprague Dawley (SD) rats

in-vitro,

Nor,

NRK52E

*antiOx↑, Allicin may exert anti-apoptotic and antioxidative effects to promote renal function recovery in I/R renal tissues and H/R treated NRK-52E cells.
*RenoP↑,
*MDA↓, Allicin ameliorated the increase in MDA content and the reduction in SOD activity induced by renal IRI in groups D, E and F
*SOD↑,

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.

2657-

AL,

Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases

Review,

CardioV,

Review,

AD,

*Inflam↓, allicin integrate a broad spectrum of properties (e.g., anti-inflammatory, immunomodulatory, antibiotic, antifungal, antiparasitic, antioxidant, nephroprotective, neuroprotective, cardioprotective, and anti-tumoral activities, among others).
*antiOx↑, improving the antioxidant system
*neuroP↑,
*cardioP↑,
*AntiTum↑,
*mtDam↑, Indeed, the current evidence suggests that allicin improves mitochondrial function by enhancing the expression of HSP70 and NRF2, decreasing RAAS activation, and promoting mitochondrial fusion processes.
*HSP70/HSPA5↑, llicin improves mitochondrial function by enhancing the expression of HSP70 and decreasing RAAS activation
*NRF2↑,
*RAAS↓,
*cognitive↑, Allicin enhances the cognitive function of APP (amyloid precursor protein)/PS1 (presenilin 1) double transgenic mice by decreasing the expression levels of Aβ, oxidative stress, and improving mitochondrial function.
*SOD↑, positive effects on cognition in an AD mouse model by administrating a preventive dose of allicin. These effects might be mediated by an increase of SOD and reduction of ROS
*ROS↓,
*NRF2↑, Chronic treatment with allicin increased the expression of NRF2 and targeted downstream of NRF2, such as NADPH, quinone oxidoreductase 1 (NQO1), and Î³-glutamyl cysteine synthetase (Î³-GCS), in the hippocampus of aged mice
*ER Stress↓, protective effects of 16 weeks of allicin treatment in a rat model of endoplasmic reticulum stress-related cognitive deficits.
*neuroP↑, allicin was able to ameliorate depressive-like behaviors by decreasing neuroinflammation, oxidative stress iron aberrant accumulation,
*memory↑, allicin improved lead acetate-caused learning and memory deficits and decreased the ROS level
*TBARS↓, Oral administration of allicin was able to reduce thiobarbituric reactive substances (TBARS) and myeloperoxidase (MPO) levels, and concurrently increased (SOD) activity, glutathione S-transferase (GST) and glutathione (GSH) levels in a rat model of
*MPO↓,
*SOD↑,
*GSH↑,
*iNOS↓, decreasing the expression of iNOS and increased the phosphorylation of endothelial NOS (eNOS)
*p‑eNOS↑,
*HO-1↑, OSCs upregulate the endogenous antioxidant NRF2 and heme oxygenase-1 (HO-1)

2658-

AL,

The Toxic Effect Ways of Allicin on Different Cell Lines

Review,

Var,

*antiOx↑, The significant functional act of garlic is its anticancer, antimicrobial, antioxidant, antidiabetic, antifibrinolytic, immune enhancing, antiplatelet collected effect and its possible act in prohibiting cardiovascular illnesses
*AntiAg↑,
*cardioP↑,
Ca+2↑, Sultan et al.[34] stated that allicin is cytotoxic to monocytic leukemia cells (THP-1 cells) and stimulates calcium-linked hemolysis and eryptosis in human red blood cells. Allicin advances calcium grades in cells, reasons to oxidative stress and al
ROS↑, Allicin advances calcium grades in cells, reasons to oxidative stress and also induces CK1a, caspase, p38, mitogen-activated protein kinase
Casp↑,
p38↑,
MAPK↑,
hepatoP↑, Wu et al.[42] clarified that allicin applies hepaprotective action counter to hepatic toxicity of cells
chemoP↑, Throughout with other garlic preparations, aged garlic extract (AGE) has been indicated to have hepatoprotective, immune, improving, anticancer, and chemoprotective actions.

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↓,

2667-

AL,

Allicin in Digestive System Cancer: From Biological Effects to Clinical Treatment

Review,

GC,

AntiCan↑, Allicin not only protects against tumors but also alleviates the adverse effects of anticancer treatment and enhances the chemotherapeutic response under certain conditions.
ChemoSen↑,
angioG↓, DATS works against tumors by blocking the cell cycle, inhibiting tumor cell proliferation, and inhibiting angiogenesis
chemoP↑,
*GutMicro↑, In addition to against bacteria, allicin has also been shown to modulate the composition of gut microbiota (GM) and increase the diversity of beneficial bacteria in animal models
*antiOx↑, allicin was confirmed to have strong antioxidant properties
other↝, Allicin is a reactive sulfur species (RSS) and a potent thiol-trapping reagent, rapidly reacting with glutathione (GSH) to yield S-allylmercaptoglutathione (GSSA)
GSH↓, Thus, allicin depletes the intracellular GSH pool and reacts with cysteine thiols available in proteins through S-thioallylation
Thiols↓, This reaction is the key to the biological activity of allicin, and the reversible oxidation and reduction of protein-thiols is the core of many processes in cells
*ROS↓, In a hypertrophic heart mouse model, the clearance of intracellular ROS by allicin was measured, and has been shown to reduce the production of ROS and block ROS-dependent ERK1/2, JNK1/2, AKT, NF-κB and Smad signaling, which leads to the inhibition o
*hepatoP↑, Moreover, allicin has been proven to play a hepatoprotective role against acetaminophen (APAP)-induced liver injury by reducing oxidative stress
*Inflam↓, OSCs in garlic has been shown to inhibit the tumor-mediated pro-inflammatory activity by modulating the cytokine pattern in a way that leads to an overall inhibition of NF-κB
*NF-kB↓,

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

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↓,

3271-

ALA,

Decrypting the potential role of α-lipoic acid in Alzheimer's disease

Review,

AD,

*antiOx↑, Alpha-lipoic acid (α-LA), a natural antioxidant
*memory↑, multiple preclinical studies indicating beneficial effects of α-LA in memory functioning, and pointing to its neuroprotective effects
*neuroP↑, α-LA could be considered neuroprotective
*Inflam↓, α-LA shows antioxidant, antiapoptotic, anti-inflammatory, glioprotective, metal chelating properties in both in vivo and in vitro studies.
*IronCh↑, α-LA leads to a marked downregulation in iron absorption and active iron reserve inside the neuron
*NRF2↑, α-LA induces the activity of the nuclear factor erythroid-2-related factor (Nrf2), a transcription factor.
*BBB↑, capable of penetrating the BBB
*GlucoseCon↑, Fig 2, α-LA mediated regulation of glucose uptake
*Ach↑, α-LA may show its action on the activity of the ChAT enzyme, which is an essential enzyme in acetylcholine metabolism
*ROS↓,
*p‑tau↓, decreased degree of tau phosphorylation following treatment with α-LA
*Aβ↓, α-LA possibly induce the solubilization of Aß plaques in the frontal cortex
*cognitive↑, cognitive reservation of α-LA served AD model was markedly upgraded in additional review
*Hif1a↑, α-LA treatment efficaciously induces the translocation and activity of hypoxia-inducible factor-1α (HIF-1α),
*Ca+2↓, research found that α-LA therapy remarkably declines Ca2+ concentration and calpain signaling
*GLUT3↑, inducing the downstream target genes expression, such as GLUT3, GLUT4, HO-1, and VEGF.
*GLUT4↑,
*HO-1↑,
*VEGF↑,
*PDKs↓, α-LA also ameliorates survival in mutant mice of Huntington's disease [150–151], possibly due to the inhibition of the activity of pyruvate dehydrogenase kinase
*PDH↑, α-LA administration enhances PDH expression in mitochondrial hepatocytes by inhibiting the pyruvate dehydrogenase kinase (PDK),
*VCAM-1↓, α-LA inhibits the expression of cell-cell adhesion molecule-1 and VCAM-1 in spinal cords and TNF-α induced neuronal endothelial cells injury
*GSH↑, α-LA may enhance glutathione production in old-aged models
*NRF2↑, activation of the Nrf2 signaling by α-LA
*hepatoP↑, α-LA also protected the liver against oxidative stress-mediated hepatotoxicity
*ChAT↑, α-LA in mice models may prevent neuronal injury possibly due to an increase in ChAT in the hippocampus of animal models

3272-

ALA,

Alpha-lipoic acid as a dietary supplement: Molecular mechanisms and therapeutic potential

Review,

AD,

*antiOx↑, LA has long been touted as an antioxidant,
*glucose↑, improve glucose and ascorbate handling,
*eNOS↑, increase eNOS activity, activate Phase II detoxification via the transcription factor Nrf2, and lower expression of MMP-9 and VCAM-1 through repression of NF-kappa-B.
*NRF2↑,
*MMP9↓,
*VCAM-1↓,
*NF-kB↓,
*cardioP↑, used to improve age-associated cardiovascular, cognitive, and neuromuscular deficits,
*cognitive↑,
*eff↓, The efficiency of LA uptake was also lowered by its administration in food,
*BBB↑, LA has been shown to cross the blood-brain barrier in a limited number of studies;
*IronCh↑, LA preferentially binds to Cu2+, Zn2+ and Pb2+, but cannot chelate Fe3+, while DHLA forms complexes with Cu2+, Zn2+, Pb2+, Hg2+ and Fe3+
*GSH↑, LA markedly increases intracellular glutathione (GSH),
*PKCδ↑, PKCδ, LA activates Erk1/2 [92,93], p38 MAPK [94], PI3 kinase [94], and Akt
*ERK↑,
*p38↑,
*MAPK↑,
*PI3K↑,
*Akt↑,
*PTEN↓, LA decreases the activities of Protein Tyrosine Phosphatase 1B [99], Protein Phosphatase 2A [95], and the phosphatase and tensin homolog PTEN [95],
*AMPK↑, LA activates peripheral AMPK
*GLUT4↑, stimulate GLUT4 translocation
*GLUT1↑, LA-stimulated translocation of GLUT1 and GLUT4.
*Inflam↓, LA as an anti-inflammatory agent

3283-

ALA,

Alpha-lipoic acid inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in human aortic endothelial cells

in-vitro,

Nor,

*TNF-α↓, LA also strongly inhibited TNF-alpha-induced mRNA expression of monocyte chemoattractant protein-1
*NF-kB↓, LA dose-dependently inhibited TNF-alpha-induced IkappaB kinase activation, subsequent degradation of IkappaB, the cytoplasmic NF-kappaB inhibitor, and nuclear translocation of NF-kappaB.
*antiOx↑, LA in its free, non-protein-bound form has potent antioxidant and metal-chelating properties
*IronCh↑,
*GSSG↓, DHLA/LA couple may chemically reduce glutathione disulfide (GSSG) to GSH
*VCAM-1↓, E-selectin, VCAM-1, ICAM-1, and MCP-1 message levels decreased by 93%, 77%, 67%, and 100%, respectively, when HAEC were pretreated with 0.5mmol/l LA
*E-sel↓,
*ICAM-1↓,
*MCP1↓,
*NF-kB↓, Lipoic acid inhibits TNF-a-induced activation of NF-kB and degradation of IkBs
IKKα↓,

3284-

ALA,

Alpha-Lipoic Acid Mediates Clearance of Iron Accumulation by Regulating Iron Metabolism in a Parkinson's Disease Model Induced by 6-OHDA

vitro+vivo,

Park,

*antiOx↑, naturally occurring enzyme cofactor with antioxidant and iron chelator properties and has many known effects. ALA has neuroprotective effects on PD.
*IronCh↑,
*neuroP↑,
*ROS↓, decreasing the levels of intracellular reactive oxygen species and iron.
*Iron↓,
*BBB↑, ALA also provides neuroprotection against PD because it can penetrate the blood–brain barrier.
*motorD↑, ALA ameliorates motor behavior and prevents DA neuron loss in the SN of PD rat models.
*GSH↑, ALA Inhibits the Decrease in the Activity of SOD and GSH in the SN of a Rat Model of PD Induced by 6-OHDA

3456-

ALA,

Renal-Protective Roles of Lipoic Acid in Kidney Disease

Review,

NA,

*RenoP↑, We focus on various animal models of kidney injury by which the underlying renoprotective mechanisms of ALA have been unraveled
*ROS↓, ALA’s renal protective actions that include decreasing oxidative damage, increasing antioxidant capacities, counteracting inflammation, mitigating renal fibrosis, and attenuating nephron cell death.
*antiOx↑,
*Inflam↓,
*Sepsis↓, figure 1
*IronCh↑, ALA can also chelate metals such as zinc, iron, and copper and regenerate endogenous antioxidants—such as glutathione—and exogenous vitamin antioxidants—such as vitamins C and E—with minimal side effects
*BUN↓, ALA can decrease acute kidney injury by lowering serum blood urea nitrogen, creatinine levels, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β), thereby decreasing endothelin-1 vasoconstriction, neutrophil dif
*creat↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*MDA↓, pretreatment with ALA decreased MDA content and ameliorated renal oxidative stress
*NRF2↑, activate the Nrf2 signaling pathway, leading to upregulation of the second-phase cytoprotective proteins such as heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1)
*HO-1↑,
*NQO1↑,
*chemoP↑, ALA has also been shown to lower plasma creatinine levels and urine output, increase creatinine clearance and urine osmolality, and normalize sodium excretion in cisplatin kidney injury
*eff↑, ALA can also minimize renal toxicity induced by gold nanoparticles, which are often used as drug carriers
*NF-kB↓, Enhancing autophagy, inhibiting NF-KB, attenuating mitochondrial oxidative stress

3437-

ALA,

Revisiting the molecular mechanisms of Alpha Lipoic Acid (ALA) actions on metabolism

Review,

Var,

*IronCh↑, ALA functions as a metabolic regulator, metal chelator, and a powerful antioxidant.
*antiOx↑,
*ROS↓, It quenches reactive oxygen species (ROS), restores exogenous and endogenous antioxidants such as vitamins and Glutathione (GSH), and repairs oxidized proteins
*GSH↑,
*NF-kB↓, inhibition of the activation of nuclear factor kappa B (NF-κB)
*AMPK⇅, activation of peripheral AMPK and inhibition of hypothalamic AMPK
*FAO↑, ALA has been found to activate peripheral AMPK, thereby enhancing fatty acid oxidation and glucose uptake in muscle cells
*GlucoseCon↑,
*PI3K↑, It stimulates glucose uptake by increasing the activity of PI3K and Akt which are crucial for the translocation of glucose transporters like GLUT4 to the cell membrane, mimicking the action of insulin
*Akt?,

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↑,

3439-

ALA,

The effect of alpha lipoic acid on the developmental competence of mouse isolated preantral follicles

in-vitro,

NA,

100uM

Pre-antral follicles were isolated from immature mouse ovaries and were cultured in α- minimal essential medium supplemented

*ROS↓, At 96 h after culture, a decrease in ROS and an increase in TAC were observed in ALA group compared to control group (p < 0.05).
*TAC↑,
*eff↑, ALA (100 uM) improves the in vitro development of follicles. This effect may be mediated by decreasing ROS concentration and increasing follicular TAC level during the culture period.‎‎‎
*SOD↑, ALA administration significantly elevated plasma total antioxidant status and could increase activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) in the brain tissues of male rat exposed to restraint stress
*GPx↑,
*Catalase↑,
*GlucoseCon↑, ALA enhances glucose uptake by cells,
*antiOx↑, Taken together, our study indicates that ALA has an excellent antioxidant activity,

3443-

ALA,

Molecular and Therapeutic Insights of Alpha-Lipoic Acid as a Potential Molecule for Disease Prevention

Review,

Var,

Review,

AD,

*antiOx↑, antioxidant potential and free radical scavenging activity.
*ROS↓,
*IronCh↑, Lipoic acid acts as a chelating agent for metal ions, a quenching agent for reactive oxygen species, and a reducing agent for the oxidized form of glutathione and vitamins C and E.
*cognitive↑, α-Lipoic acid enantiomers and its reduced form have antioxidant, cognitive, cardiovascular, detoxifying, anti-aging, dietary supplement, anti-cancer, neuroprotective, antimicrobial, and anti-inflammatory properties.
*cardioP↓,
AntiCan↑,
*neuroP↑,
*Inflam↓, α-Lipoic acid can reduce inflammatory markers in patients with heart disease
*BioAv↓, bioavailability in its pure form is low (approximately 30%).
*AntiAge↑, As a dietary supplements α-lipoic acid has become a common ingredient in regular products like anti-aging supplements and multivitamin formulations
*Half-Life↓, it has a half-life (t1/2) of 30 min to 1 h.
*BioAv↝, It should be stored in a cool, dark, and dry environment, at 0 °C for short-term storage (few days to weeks) and at − 20 °C for long-term storage (few months to years).
other↝, Remarkably, neither α-lipoic acid nor dihydrolipoic acid can scavenge hydrogen peroxide, possibly the most abundant second messenger ROS, in the absence of enzymatic catalysis.
EGFR↓, α-Lipoic acid inhibits cell proliferation via the epidermal growth factor receptor (EGFR) and the protein kinase B (PKB), also known as the Akt signaling, and induces apoptosis in human breast cancer cells
Akt↓,
ROS↓, α-Lipoic acid tramps the ROS followed by arrest in the G1 phase of the cell cycle and activates p27 (kip1)-dependent cell cycle arrest via changing of the ratio of the apoptotic-related protein Bax/Bcl-2
TumCCA↑,
p27↑,
PDH↑, α-Lipoic acid drives pyruvate dehydrogenase by downregulating aerobic glycolysis and activation of apoptosis in breast cancer cells, lactate production
Glycolysis↓,
ROS↑, HT-29 human colon cancer cells; It was concluded that α-lipoic acid induces apoptosis by a pro-oxidant mechanism triggered by an escalated uptake of mitochondrial substrates in oxidizable form
*eff↑, Several studies have found that combining α-lipoic acid and omega-3 fatty acids has a synergistic effect in slowing functional and cognitive decline in Alzheimer’s disease
*memory↑, α-lipoic acid inhibits brain weight loss, downregulates oxidative tissue damage resulting in neuronal cell loss, repairs memory and motor function,
*motorD↑,
*GutMicro↑, modulates the gut microbiota without reducing the microbial diversity (

3445-

ALA,

Rad,

The radioprotective effects of alpha-lipoic acid on radiotherapy-induced toxicities: A systematic review

Review,

Var,

*radioP↑, radio-protective role of alpha-lipoic acid.
*antiOx↑, Alpha-lipoic acid has anti-oxidant, anti-apoptosis, anti-inflammatory actions, etc.
*Inflam↓,

3444-

ALA,

Alpha-Lipoic Acid Nootropic Review: Benefits, Use, Dosage & Side Effects

Review,

NA,

*BBB↑, ALA's ability to cross the blood-brain barrier and its dual solubility in both water and lipid environments position it as a promising compound in the realm of cognitive enhancement and neurological health
*cognitive↑,
*neuroP↑, Alpha-lipoic acid demonstrates robust neuroprotective and cognitive-enhancing effects through its potent antioxidant properties
*antiOx↑,

3449-

ALA,

Alpha-Lipoic Acid Downregulates IL-1β and IL-6 by DNA Hypermethylation in SK-N-BE Neuroblastoma Cells

in-vitro,

AD,

SK-N-BE

*antiOx↑, ability to maintain its antioxidant properties both in its oxidised and reduced form
*NRF2↑, Antioxidant action of ALA is mediated by two essential nuclear factors: nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa-light chain-enhancer of activated B cells (NF-kB) [5,6,7,8,9,10]
*NF-kB↓,
*IL1β↓, ALA-dependent down-regulation of IL-1β and IL-6 in neuronal cells.
*IL6↓,
neuroP↑, ALA was already indicated as a potential therapeutic agent in aging-associated neurodegenerative disorders

3551-

ALA,

Alpha lipoic acid treatment in late middle age improves cognitive function: Proteomic analysis of the protective mechanisms in the hippocampus

in-vivo,

AD,

mice

*cognitive↑, ALA improves cognitive function in ageing mice.
*Apoptosis↓, ALA downregulates apoptosis, and neuroinflammatory associated proteins in ageing mice.
*Inflam↓,
*antiOx↑, Alpha lipoic acid (ALA), a powerful antioxidant, has the potential to relieve age-related cognitive impairment and neurodegenerative disease.
*BioAv↝, Alpha lipoic acid (ALA) is a sulfur-containing and both water-soluble and lipid-soluble coenzyme involved in the energy metabolism of carbohydrates, proteins and lipids
*neuroP↑, neuroprotective action of alpha lipoic acid has been demonstrated in a number of cellular or animal models of Parkinson's disease (PD), AD and amyotrophic lateral sclerosis (ALS) due to its antioxidative and anti-inflammatory properties

3539-

ALA,

Alpha-lipoic acid as a dietary supplement: Molecular mechanisms and therapeutic potential

Review,

AD,

*ROS↓, scavenges free radicals, chelates metals, and restores intracellular glutathione levels which otherwise decline with age.
*IronCh↑, LA preferentially binds to Cu2+, Zn2+ and Pb2+, but cannot chelate Fe3+, while DHLA forms complexes with Cu2+, Zn2+, Pb2+, Hg2+ and Fe3+
*GSH↑,
*antiOx↑, LA has long been touted as an antioxidant
*NRF2↑, activate Phase II detoxification via the transcription factor Nrf2
*MMP9↓, lower expression of MMP-9 and VCAM-1 through repression of NF-kappa-B.
*VCAM-1↓,
*NF-kB↓,
*cognitive↑, it has been used to improve age-associated cardiovascular, cognitive, and neuromuscular deficits, and has been implicated as a modulator of various inflammatory signaling pathways
*Inflam↓,
*BioAv↝, LA bioavailability may be dependent on multiple carrier proteins.
*BioAv↝, observed that approximately 20-40% was absorbed [
*BBB↑, LA has been shown to cross the blood-brain barrier in a limited number of studies
*H2O2∅, Neither species is active against hydrogen peroxide
*neuroP↑, chelation of iron and copper in the brain had a positive effect in the pathobiology of Alzheimer’s Disease by lowering free radical damage
*PKCδ↑, In addition to PKCδ, LA activates Erk1/2 [92, 93], p38 MAPK [94], PI3 kinase [94], and Akt [94-97].
*ERK↑,
*MAPK↑,
*PI3K↑,
*Akt↑,
*PTEN↓, LA decreases the activities of Protein Tyrosine Phosphatase 1B [99], Protein Phosphatase 2A [95], and the phosphatase and tensin homolog PTEN
*AMPK↑, LA activates peripheral AMPK
*GLUT4↑, In skeletal muscle, LA is proposed to recruit GLUT4 from its storage site in the Golgi to the sarcolemma, so that glucose uptake is stimulated by the local increase in transporter abundance.
*GlucoseCon↑,
*BP↝, Feeding LA to hypertensive rats normalized systolic blood pressure and cytosolic free Ca2+
*eff↑, Clinically, LA administration (in combination with acetyl-L-carnitine) showed some promise as an antihypertensive therapy by decreasing systolic pressure in high blood pressure patients and subjects with the metabolic syndrome
*ICAM-1↓, decreased demyelination and spinal cord expression of adhesion molecules (ICAM-1 and VCAM-1)
*VCAM-1↓,
*Dose↝, Considering the transient cellular accumulation of LA following an oral dose, which does not exceed low micromolar levels, it is entirely possible that some of the cellular effects of LA when given at supraphysiological concentrations may be not be c

3541-

ALA,

Insights on alpha lipoic and dihydrolipoic acids as promising scavengers of oxidative stress and possible chelators in mercury toxicology

Review,

Var,

*antiOx↑, Î±-LA has been widely used as an antioxidant compound in many multivitamin formulations, food supplements, anti-aging formulas, and even in human and pet food recipes
*IronCh↑, potential role in the chelation of metals and in restoring normal levels of intracellular glutathione (GSH) after depletion caused by toxicants,
*GSH↑,
*BBB↑, ALA, which can pass through the blood-brain barrier (BBB
Apoptosis↑, increased level of apoptosis, mitochondrial membrane depolarization, ROS production, lipid peroxidation, poly-(ADP)-ribose polymerase 1 (PARP1), caspase 3 and 9 expression levels in simultaneous ALA (0.05 mM) and cisplatin(0.025 mM)-treated MCF7
MMP↓,
ROS↑,
lipid-P↑,
PARP1↑,
Casp3↑,
Casp9↑,
*NRF2↑, ALA's ability to activate Nfr2 in GSH production
*GSH↑,
*ROS↓, administration of ALA has been shown to reduce oxidative stress
RenoP↑, ALA also reduced lipid peroxidation in the kidneys caused by the anticancer drug cisplatin,
ChemoSen↑, ALA enhances the functions of various anticancer drugs such as 5-fluorouracil in CRC [146] and cisplatin in MCF-7 cells
*BG↓, ALA was shown to lower the blood glucose levels in patients with type 2 diabetes

3542-

ALA,

Chelation: Harnessing and Enhancing Heavy Metal Detoxification—A Review

Review,

Var,

*antiOx↑, powerful antioxidant that regenerates other antioxidants (e.g., vitamins E and C, and reduced glutathione) and has metal-chelating activity.
*VitE↑,
*VitC↑,
*GSH↑,
*IronCh↑,
*BioAv↑, Both fat and water soluble, it is readily absorbed from the gut and crosses cellular and blood-brain membrane barriers
*BBB↑,

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↑,

3550-

ALA,

Mitochondrial Dysfunction and Alpha-Lipoic Acid: Beneficial or Harmful in Alzheimer's Disease?

Review,

AD,

*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓,
*PGE2↓, α-LA has mechanisms of epigenetic regulation in genes related to the expression of various inflammatory mediators, such PGE2, COX-2, iNOS, TNF-α, IL-1β, and IL-6
*COX2↓,
*iNOS↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*BioAv↓, α-LA has rapid uptake and low bioavailability and the metabolism is primarily hepatic
*Ach↑, α-LA increases the production of acetylcholine [30], inhibits the production of free radicals [31], and promotes the downregulation of inflammatory processes
*ROS↓,
*cognitive↑, Studies have shown that patients with mild AD who were treated with α-LA showed a slower progression of cognitive impairment
*neuroP↑, α-LA is classified as an ideal neuroprotective antioxidant because of its ability to cross the blood-brain barrier and its uniform uptake profile throughout the central and peripheral nervous systems
*BBB↑,
*Half-Life↓, α-LA presented a mean time to reach the maximum plasma concentration (tmax) of 15 minutes and a mean plasma half-life (t1/2) of 14 minutes
*BioAv↑, LA consumption is recommended 30 minutes before or 2 hours after food intake
*Casp3↓, α-LA had an effect on caspases-3 and -9, reducing the activity of these apoptosis-promoting molecules to basal levels
*Casp9↓,
*ChAT↑, α-LA increased the expression of M2 muscarinic receptors in the hippocampus and M1 and M2 in the amygdala, in addition to ChaT expression in both regions.
*cognitive↑, α-LA acts on these apoptotic signalling pathways, leading to improved cognitive function and attenuation of neurodegeneration.
*eff↑, Based on their results, the authors suggest that treatment with α-LA would be a successful neuroprotective option in AD, at least as an adjuvant to standard treatment with acetylcholinesterase inhibitors.
*cAMP↑, The increase of cAMP caused by α-LA inhibits the release of proinflammatory cytokines, such as IL-2, IFN-γ, and TNF-α.
*IL2↓,
*INF-γ↓,
*TNF-α↓,
*SIRT1↑, Protein expression encoded by SIRT1 showed higher levels after α-LA treatment, especially in liver cells.
*SOD↑, antioxidant enzymes (SOD and GSH-Px) and malondialdehyde (MDA) were analysed by ELISA after 24 h of MCAO, which showed that the enzymatic activities were recovered and MDA was reduced in the α-LA-treated groups i
*GPx↑,
*MDA↓,
*NRF2↑, The ratio of nucleus/cytoplasmic Nrf2 was higher in the α-LA group 40 mg/kg, indicating that the activation of this factor also occurred in a dose-dependent manner

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

3544-

ALA,

Alpha lipoic acid for dementia

Review,

AD,

*antiOx↑, ALA is a low molecular weight antioxidant, readily absorbed from the diet or an oral dose, and crosses the blood brain barrier
*BBB↑,
*VitC↑, DHLA regenerates through redox cycling other antioxidants like vitamin C and E and raises levels of intracellular glutathione, an important thiol antioxidant
*VitE↑,
*GSH↑,
*IronCh↑, ALA al- so chelates certain metals, forming stable complexes with copper, manganese and zinc (Sigel 1978)
*neuroP↑, ALA would seem an ideal candidate as an antioxidant agent in neurodegenerative diseases.
*NO↓, ALA also modulates nitric oxide levels in brain and neural tissue, which may have effects in neurodegeneration, learning, cognition, and aging (Gross 1995)
*cognitive↑, elderly patients with dementia were given ALA. Findings suggested a stabilization of cognitive functions in the study group,
*AntiAge↑,
*memory↑, ALA has gained considerable attention following studies demonstrating partial reversal of memory loss in aged rats.
*ROS↓, scavenging hy- droxyl or superoxide radicals (Suzuki 1991) and by scavenging per- oxyl radicals (

278-

ALA,

The Multifaceted Role of Alpha-Lipoic Acid in Cancer Prevention, Occurrence, and Treatment

Review,

NA,

ROS↑, direct anticancer effect of the antioxidant ALA is manifested as an increase in intracellular ROS levels in cancer cells
NRF2↑, enhance the activity of the anti-inflammatory protein nuclear factor erythroid 2–related factor 2 (Nrf2), thereby reducing tissue damage
Inflam↓,
frataxin↑,
*BioAv↓, Oral ALA has a bioavailability of approximately 30% due to issues such as poor stability in the stomach, low solubility, and hepatic degradation.
ChemoSen↑, ALA can enhance the functionality of various other anticancer drugs, including 5-fluorouracil in colon cancer cells and cisplatin in MCF-7 breast cancer cells
Hif1a↓, it is inferred that lipoic acid may inhibit the expression of HIF-1α
eff↑, act as a synergistic agent with natural polyphenolic substances such as apigenin and genistein
FAK↓, ALA inhibits FAK activation by downregulating β1-integrin expression and reduces the levels of MMP-9 and MMP-2
ITGB1↓,
MMP2↓,
MMP9↓,
EMT↓, ALA inhibits the expression of EMT markers, including Snail, vimentin, and Zeb1
Snail↓,
Vim↓,
Zeb1↓,
P53↑, ALA also stimulates the mutant p53 protein and depletes MGMT
MGMT↓, depletes MGMT by inhibiting NF-κB signalling, thereby inducing apoptosis
Mcl-1↓,
Bcl-xL↓,
Bcl-2↓,
survivin↓,
Casp3↑,
Casp9↑,
BAX↑,
p‑Akt↓, ALA inhibits the activation of tumour stem cells by reducing Akt phosphorylation.
GSK‐3β↓, phosphorylation and inactivation of GSK3β
*antiOx↑, indirect antioxidant protection through metal chelation (ALA primarily binds Cu2+ and Zn2+, while DHLA can bind Cu2+, Zn2+, Pb2+, Hg2+, and Fe3+) and the regeneration of certain endogenous antioxidants, such as vitamin E, vitamin C, and glutathione
*ROS↓, ALA can directly quench various reactive species, including ROS, reactive nitrogen species, hydroxyl radicals (HO•), hypochlorous acid (HclO), and singlet oxygen (1O2);
selectivity↑, In normal cells, ALA acts as an antioxidant by clearing ROS. However, in cancer cells, it can exert pro-oxidative effects, inducing pathways that restrict cancer progression.
angioG↓, Combining these two hypotheses, it can be hypothesized that ALA may regulate copper and HIF-2α to limit tumor angiogenesis.
MMPs↓, ALA was shown to inhibit invasion by decreasing the mRNA levels of key matrix metalloproteinases (MMPs), specifically MMP2 and MMP9, which are crucial for the metastatic process
NF-kB↓, ALA has been shown to enhance the efficacy of the chemotherapeutic drug paclitaxel in breast and lung cancer cells by inhibiting the NF-κB signalling pathway and the functions of integrin β1/β3 [138,139]
ITGB3↓,
NADPH↓, ALA has been shown to inhibit NADPH oxidase, a key enzyme closely associated with NP, including NOX4

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↑,

5262-

aLinA,

The Role of Alpha-Linolenic Acid and Other Polyunsaturated Fatty Acids in Mental Health: A Narrative Review

Review,

AD,

*neuroP↑, The evidence suggests that PUFAs are beneficial for mental health, brain function, and behavior. ALA, EPA, and DHA have very significant neuroprotective properties, particularly in inducing changes to the synaptic membrane and modulating brain cell s
*Risk↓, DHA is a primary component of neuronal membranes in regions critical to memory and cognition, such as the hippocampus and cortex, and low levels of DHA are associated with an increased risk of cognitive decline [16,22].
*cognitive↑, Omega-3 supplementation has shown promise in delaying cognitive decline and neurodegeneration, potentially due to its anti-inflammatory and antioxidative properties, as well as its role in neurogenesis and brain-derived neurotrophic factor (BDNF) enh
*Inflam↓,
*antiOx↑,
*BDNF↑,

4279-

Api,

The Beneficial Role of Apigenin against Cognitive and Neurobehavioural Dysfunction: A Systematic Review of Preclinical Investigations

Review,

NA,

Most studies used 10, 20, 40, 50 and 100 mg/kg

*antiOx↑, potent antioxidant and has been shown to exhibit anti-inflammatory, antitumorigenic and antimicrobial activities
*Inflam↓,
*BBB↑, Its ability to cross the blood–brain barrier is important as it contributes to its pharmacological activity against neurological disorders
*5HT↑, Apigenin improved serotonin, dopamine and epinephrine levels, which were altered in depressive animals
*CREB↑, Apigenin further regulates the cAMP-CREB-BDNF signalling pathway and N-methyl-D-aspartate (NMDA) receptors, which play important roles in neuronal survival, synaptic plasticity, cognitive function and mood behaviour
*BDNF↑, Apigenin improved BDNF levels and enhanced ERK1/2 and CREB expression
*memory↑, All the studies showed that apigenin improved learning and memory, except for two studies.
*motorD↑, In the open field test, apigenin improved locomotor activity
*Mood↑, The splash test revealed that apigenin improved grooming activity and locomotion in streptozotocin-induced depressive-like behaviour in a mouse model via an improvement in grooming activity.
*cognitive↑, The studies included in this systematic review showed that apigenin improved cognitive function and neurobehaviour in impaired or stressed animals.
*ROS↓, inhibition of ROS production

4280-

Api,

Protective effects of apigenin in neurodegeneration: An update on the potential mechanisms

Review,

AD,

Review,

Park,

*neuroP↑, Apigenin, a flavonoid found in various herbs and plants, has garnered significant attention for its neuroprotective properties
*antiOx↑, shown to possess potent antioxidant activity, which is thought to play a crucial role in its neuroprotective effects
*ROS↓, Apigenin has been demonstrated to scavenge ROS, thereby reducing oxidative stress and mitigating the damage to neurons
*Inflam↓, apigenin has been found to possess anti-inflammatory properties.
*TNF-α↓, inhibit the production of pro-inflammatory cytokines, such as TNF-α and IL-1β, which are elevated in neurodegenerative diseases
*IL1β↓,
*PI3K↑, apigenin has been shown to activate the PI3K/Akt signaling pathway, which is involved in promoting neuronal survival and preventing apoptosis.
*Akt↑,
*BBB↑, Apigenin has additional neuroprotective properties due to its ability to cross the BBB and enter the brain
*NRF2↑, figure 1
*SOD↑, pigenin has also been shown to activate various antioxidant enzymes, such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx)
*GPx↑,
*MAPK↓, Apigenin inhibits the MAPK signalling system, which significantly reduces oxidative stress-induced damage in the brain
*Catalase↑, , including SOD, catalase, GPx and heme oxygenase-1 (HO-1) [37].
*HO-1↑,
*COX2↓, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*PGE2↓,
*PPARγ↑, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*TLR4↓,
*GSK‐3β↓, Apigenin can inhibit the activity of GSK-3β,
*Aβ↓, Inhibiting GSK-3 can reduce Aβ production and prevent neurofibrillary disorders.
*NLRP3↓, Apigenin suppresses nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) inflammasome activation by upregulating PPAR-γ
*BDNF↑, Apigenin causes upregulation of BDNF and TrkB expression in several animal models
*TrkB↑,
*GABA↑, Apigenin enhances GABAergic signaling by increasing the frequency of chloride channel opening, leading to increased inhibitory neurotransmission
*AChE↓, It blocks acetylcholinesterase and increases acetylcholine availability.
*Ach↑,
*5HT↑, Apigenin has been shown to increase 5-HT levels, decrease 5-HT turnover, and prevent dopamine changes.
*cognitive↑, Apigenin increases the availability of acetylcholine in the synapse after inhibiting AChE, thereby enhancing cholinergic neurotransmission and improving cognitive function and memory
*MAOA↓, apigenin acts as a monoamine oxidase (MAO) inhibitor and MAO inhibitors increase the levels of monoamines in the brain

Showing Research Papers: 1 to 50 of 592
Page 1 of 12 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 592

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 98

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 47, Catalase↑, 7, GPx↑, 4, GSH↑, 20, GSR↑, 1, GSSG↓, 1, GSTs↑, 3, H2O2∅, 1, HO-1↑, 4, Iron↓, 1, Keap1↓, 1, lipid-P↓, 9, MDA↓, 6, MPO↓, 3, NQO1↑, 2, Nrf1↑, 1, NRF2↑, 13, ROS↓, 25, ROS↑, 1, SOD↑, 9, TAC↑, 1, TBARS↓, 2, VitC↑, 3, VitE↑, 3,

Metal & Cofactor Biology ⓘ

IronCh↑, 14,

Mitochondria & Bioenergetics ⓘ

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

Core Metabolism/Glycolysis ⓘ

ACC↑, 1, Acetyl-CoA↑, 3, adiP↑, 1, ALAT↓, 2, AMPK↑, 2, AMPK⇅, 1, BUN↓, 1, cAMP↑, 1, CREB↑, 1, FAO↑, 1, glucose↓, 1, glucose↑, 1, GlucoseCon↑, 8, H2S↑, 2, LDH↓, 3, LDL↓, 1, NADPH↑, 1, PDH↑, 1, PDKs↓, 1, PPARγ↑, 1, SIRT1↑, 2,

Cell Death ⓘ

Akt?, 1, Akt↓, 1, Akt↑, 3, Apoptosis↓, 2, Casp3↓, 1, Casp9↓, 1, Cyt‑c↓, 1, iNOS↓, 5, JNK↓, 1, MAPK↓, 1, MAPK↑, 2, p38↑, 1,

Transcription & Epigenetics ⓘ

Ach↑, 7, other↓, 1, other↑, 1, other↝, 1,

Protein Folding & ER Stress ⓘ

ER Stress↓, 1, HSP70/HSPA5↑, 1,

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 2, GSK‐3β↓, 1, PI3K↓, 1, PI3K↑, 4, PTEN↓, 2,

Migration ⓘ

AntiAg↑, 2, APP↓, 1, Ca+2↓, 2, Ca+2↝, 1, E-sel↓, 1, MMP9↓, 2, PKCδ↑, 3, VCAM-1↓, 6,

Angiogenesis & Vasculature ⓘ

eNOS↑, 1, p‑eNOS↑, 1, Hif1a↑, 1, NO↓, 4, VEGF↓, 1, VEGF↑, 1,

Barriers & Transport ⓘ

BBB↑, 15, GLUT1↑, 1, GLUT3↑, 1, GLUT4↑, 3,

Immune & Inflammatory Signaling ⓘ

COX2↓, 3, ICAM-1↓, 2, IL1β↓, 5, IL2↓, 1, IL6↓, 5, Imm↑, 1, INF-γ↓, 1, Inflam↓, 23, MCP1↓, 1, NF-kB↓, 13, p‑NF-kB↓, 1, PGE2↓, 3, TLR4↓, 2, TNF-α↓, 7,

Cellular Microenvironment ⓘ

NOX↓, 1,

Synaptic & Neurotransmission ⓘ

5HT↑, 3, AChE↓, 2, BDNF↑, 4, ChAT↑, 6, GABA↑, 1, MAOA↓, 1, p‑tau↓, 1, TrkB↑, 1,

Protein Aggregation ⓘ

Aβ↓, 6, BACE↓, 1, NLRP3↓, 1,

Hormonal & Nuclear Receptors ⓘ

RAAS↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 3, BioAv↑, 5, BioAv↝, 6, Dose↝, 3, eff?, 1, eff↓, 1, eff↑, 7, Half-Life↓, 4, Half-Life↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 2, AST↓, 2, BG↓, 1, BP↓, 3, BP↝, 1, creat↓, 2, GutMicro↑, 3, IL6↓, 5, LDH↓, 3,

Functional Outcomes ⓘ

AntiAge↑, 3, AntiCan↑, 2, AntiDiabetic↑, 2, AntiTum↑, 1, cardioP↓, 1, cardioP↑, 7, chemoP↑, 1, cognitive↑, 20, cognitive∅, 2, hepatoP↑, 5, memory↑, 12, Mood↑, 2, motorD↑, 3, neuroP↑, 21, radioP↑, 1, RenoP↑, 3, Risk↓, 1, toxicity↝, 1, toxicity∅, 1, Weight↓, 2,

Infection & Microbiome ⓘ

Bacteria↓, 1, Sepsis↓, 1,
Total Targets: 160

Scientific Paper Hit Count for: antiOx, anti-oxidant activities

36 Lycopene
27 Curcumin
25 Alpha-Lipoic-Acid
25 Thymoquinone
24 Resveratrol
24 Selenium NanoParticles
22 Quercetin
18 Rosmarinic acid
18 Hydrogen Gas
17 Silymarin (Milk Thistle) silibinin
16 Astaxanthin
14 Chlorogenic acid
13 Silver-NanoParticles
13 Ferulic acid
12 Carvacrol
12 Honokiol
11 Baicalein
11 Berberine
11 Propolis -bee glue
11 EGCG (Epigallocatechin Gallate)
10 Vitamin C (Ascorbic Acid)
9 Coenzyme Q10
9 Magnetic Fields
9 Moringa oleifera
8 Allicin (mainly Garlic)
8 Selenium
8 Luteolin
7 Apigenin (mainly Parsley)
7 chitosan
7 Sulforaphane (mainly Broccoli)
6 Radiotherapy/Radiation
6 Melatonin
6 Capsaicin
6 Fisetin
6 Magnolol
6 Urolithin
5 Ashwagandha(Withaferin A)
5 Boron
5 Thymol-Thymus vulgaris
5 Carnosine
5 Chemotherapy
5 Vitamin E
4 Betulinic acid
4 beta-carotene(VitA)
4 Bacopa monnieri
4 Caffeic acid
4 Caffeic Acid Phenethyl Ester (CAPE)
4 Chrysin
4 Cinnamon
4 Crocetin
4 Shilajit/Fulvic Acid
4 Piperine
4 Pterostilbene
4 Shikonin
4 Selenite (Sodium)
3 Ascorbyl Palmitate
3 Vitamin K2
3 Ellagic acid
3 Ginkgo biloba
3 HydroxyTyrosol
3 Lecithin
3 Rutin
3 Salvia officinalis
3 Taurine
3 Ursolic acid
2 Anthocyanins
2 doxorubicin
2 Aromatherapy
2 Cisplatin
2 Vitamin B6,pyridoxine
2 Chocolate
2 Ginger/6-Shogaol/Gingerol
2 Hydroxycinnamic-acid
2 Huperzine A/Huperzia serrata
2 Methylene blue
2 Phenylbutyrate
2 Phenethyl isothiocyanate
2 Propyl gallate
2 Shankhpushpi
2 Vitamin B1/Thiamine
2 Vitamin B12
2 Folic Acid, Vit B9
2 Vitamin D3
1 Astragalus
1 Citric Acid
1 Ajoene (compound of Garlic)
1 alpha Linolenic acid
1 Artemisinin
1 Aloe anthraquinones
1 beta-glucans
1 Baicalin
1 Biochanin A
1 Boswellia (frankincense)
1 Bruteridin(bergamot juice)
1 Carnosic acid
1 Celastrol
1 Chlorophyllin
1 Choline
1 Copper and Cu NanoParticles
1 diet Methionine-Restricted Diet
1 Fenbendazole
1 flavonoids
1 Gallic acid
1 hydrogen sulfide
1 Juglone
1 Lutein
1 Magnetic Field Rotating
1 Methylsulfonylmethane
1 N-Acetyl-Cysteine
1 nicotinamide adenine dinucleotide
1 Naringin
1 Phosphatidylserine
1 Psoralidin
1 Perilla
1 Sulfasalazine
1 Date Fruit Extract
1 Sesame seeds and Oil
1 Iron
1 Spermidine
1 Ginseng
1 Aflavin-3,3′-digallate
1 Dichloroacetate
1 probiotics
1 Zinc

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#:1103  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

antiOx Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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