NO Cancer Research Results

NO, Nitric Oxide: Click to Expand ⟱
Source:
Type:
Once the cancer has begun, NO seems to play a protumoral role rather than antitumoral one as the concentration required to cause tumor cell cytotoxicity cannot be achieved by cancer cells.
The mechanistic roles of nitric oxide (NO) during cancer progression have been important considerations since its discovery as an endogenously generated free radical. Nonetheless, the impacts of this signaling molecule can be seemingly contradictory, being both pro-and antitumorigenic, which complicates the development of cancer treatments based on the modulation of NO fluxes in tumors. At a fundamental level, low levels of NO drive oncogenic pathways, immunosuppression, metastasis, and angiogenesis, while higher levels lead to apoptosis and reduced hypoxia and also sensitize tumors to conventional therapies. However, clinical outcome depends on the type and stage of the tumor as well as the tumor microenvironment.
Nitric oxide is generated by three main nitric oxide synthase isoforms: neuronal (nNOS), endothelial (eNOS), and inducible (iNOS).

– In many cancers, especially under inflammatory conditions, iNOS expression is upregulated. In contrast, eNOS levels may also be altered in cancers such as breast or prostate cancer.

• Expression Patterns in Tumors:
– Elevated iNOS expression is commonly observed in various tumor types (e.g., colon, breast, lung, and melanoma) and is often associated with an inflammatory microenvironment.

– Changes in eNOS and nNOS expression have also been reported and may contribute to angiogenesis and tumor blood flow regulation.
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, NA - Review, Var, NA
*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.

3972- ACNs,    Recent Research on the Health Benefits of Blueberries and Their Anthocyanins
- Review, AD, NA - Review, Park, NA
*cardioP↑, Epidemiological studies associate regular, moderate intake of blueberries and/or anthocyanins with reduced risk of cardiovascular disease, death, and type 2 diabetes, and with improved weight maintenance and neuroprotection.
*neuroP↑,
*Inflam↓, Among the more important healthful aspects of blueberries are their anti-inflammatory and antioxidant actions and their beneficial effects on vascular and glucoregulatory function
*antiOx↓,
*GutMicro↑, Blueberry phytochemicals may affect gastrointestinal microflora and contribute to host health
*Half-Life↑, However, >50% of the 13C still remained in the body after 48 h
*LDL↓, controlled study of 58 diabetic patients, blueberry intake led to a decline in LDL cholesterol, triglycerides, and adiponectin and an increase in HDL cholesterol
*adiP↓,
*HDL↑,
*CRP↓, reduction was documented in inflammatory markers, including serum high-sensitivity C-reactive protein, soluble vascular adhesion molecule-1, and plasma IL-1β
*IL1β↓,
*Risk↓, lower Parkinson disease risk was associated with the highest quintile of anthocyanin (RR: 0.76) and berry (RR: 0.77) intake
*Risk↓, Nurse's Health Study, greater intake of blueberries and strawberries was associated with slower rates of cognitive decline in older adults, with an estimated delay in decline of about 2.5 y
*cognitive↑, Cognitive performance in elderly adults improved after 12 wk of daily intake of blueberry (94) or Concord grape (95) juice.
*memory↑, Better task switching and reduced interference in memory was found in healthy older adults after 90 d of blueberry supplementation
*other↑, After 12 wk of blueberry consumption, greater brain activity was detected using magnetic resonance imaging in healthy older adults during a cognitive challenge.
*BOLD↑, Similarly, during a memory test, regional blood oxygen level-dependent activity detected by MRI (99) was enhanced in the subjects taking blueberry, but not in those taking placebo.
*NO↓, 50–200 mg/d bilberry showed a dose-dependent decrease in neurotoxic NO and malondialdehyde, combined with an increase in neuroprotective antioxidant capacity due to glutathione, vitamin C, superoxide dismutase, and glutathione peroxidase
*MDA↓,
*GSH↑,
*VitC↑,
*SOD↑,
*GPx↑,
*eff↓, The percentage loss of blueberry anthocyanins during −18°C storage was 12% after 10 mo of storage
*eff↓, Freeze-dried blueberry powder loses anthocyanins in a temperature-dependent manner with a half-life of 139, 39, and 12 d when stored at 25, 42, and 60°C, respectively
*eff↓, Blueberries are low in ascorbic acid and high in anthocyanins (187), and notably anthocyanins are readily degraded by ascorbic acid
*eff↝, Shelf-stable blueberry products like jam (196), juice (197), and extracts (198) can lose polyphenolic compounds when stored at ambient temperature whereas refrigeration mitigates losses.
*Risk↓, It can be safely stated that daily moderate intake (50 mg anthocyanins, one-third cup of blueberries) can mitigate the risk of diseases and conditions of major socioeconomic importance in the Western world.

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, NA
*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, NA
*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↑,

2660- AL,    Allicin: A review of its important pharmacological activities
- Review, AD, NA - Review, Var, NA - Review, Park, NA - Review, Stroke, NA
*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↓,

3552- ALA,    The dietary fatty acids α-linolenic acid (ALA) and linoleic acid (LA) selectively inhibit microglial nitric oxide production
- in-vitro, AD, BV2
*NO↓, ALA reduced NO without a corresponding reduction of iNOS.
*cognitive↑, select microglial immune functions by ALA and LA could be one of the mechanisms underlying the observed link between certain dietary patterns and AD, such as reduced risk of cognitive decline and dementia associated with the Mediterranean diet.

3549- ALA,    Important roles of linoleic acid and α-linolenic acid in regulating cognitive impairment and neuropsychiatric issues in metabolic-related dementia
- Review, AD, NA
*Inflam↓, LA and ALA attenuate neuroinflammation by modulating inflammatory signaling.
*other↝, ratio of LA to ALA in typical Western diets is reportedly 8–10:1 or higher, which is rather higher than the ideal ratio of LA to ALA (1–2:1) required to reach the maximal conversion of ALA to its longer chain PUFAs
*other↝, LA and ALA are essential PUFAs that must be obtained from dietary intake because they cannot be synthesized de novo
*neuroP↑, several studies have also suggested that lower dietary intake of LA influences AA metabolism in brain and subsequently causes progressive neurodegenerative disorders
*BioAv↝, LA cannot be synthesized in the human body
*adiP↑, study suggested that LA-rich oil consumption leads to the high levels of adiponectin in the blood [114], which could stimulate mitochondrial function in the liver and skeletal muscles for energy thermogenesis
*BBB↑, Although LA can penetrate the BBB, most of the LA that enters the brain cannot be changed into AA [48,49], and 59 % of the LA that enters the brain is broken down by fatty acid β-oxidation
*Casp6↓, In neurons, LA and ALA attenuate the activation of cleaved caspase-3/-9, p-NF-Kb and the production of TNF-a, IL-6, IL-1b, and ROS by binding GPR40 and GPR120.
*Casp9↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*ROS↓,
*NO↓, LA reduces NO production and inducible nitric oxide synthases (iNOS) protein expression in BV-2 microglia
*iNOS↓,
*COX2↓, ALA increases antioxidant enzyme activities in the brain [182] and inhibits the activation of COX-2 in AD models
*JNK↓, ALA has also been shown to suppress the activation of c-Jun N-terminal kinases (JNKs) and p-NF-kB p65 (Ser536), which is involved in inflammatory signaling
*p‑NF-kB↓,
*Aβ↓, and to inhibit Aβ aggregation and neuronal cell necrosis
*BP↓, LA also improves blood pressure, blood triglyceride and cholesterol levels, and vascular inflammation
*memory↑, One study suggested that long-term intake of ALA enhances memory function by increasing hippocampal neuronal function through activation of cAMP response element-binding protein (CREB) [192], extracellular signal-regulated kinase (ERK), and Akt signa
*cAMP↑,
*ERK↑,
*Akt↑,
cognitive?, Furthermore, ALA administration inhibits Aβ induced neuroinflammation in the cortex and hippocampus and enhances cognitive function

3544- ALA,    Alpha lipoic acid for dementia
- Review, AD, NA
*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 (

1253- aLinA,    The Antitumor Effects of α-Linolenic Acid
- Review, NA, NA
PPARγ↑,
COX2↓,
E6↓,
E7↓,
P53↑,
p‑ERK↓,
p38↓,
lipid-P↑,
ROS⇅, ALA could inhibit cancer by stimulating ROS production to induce apoptosis (other places implies reduced) appropriate dose of ALA can also reduce OS by regulating SOD, CAT, GPx, GSH, and NADPH oxidase
MPT↑, directly activate mitochondrial permeability transition
MMP↓,
Cyt‑c↑, cytochrome c (cyt c) release
Casp↑,
iNOS↓,
NO↓,
Casp3↑,
Bcl-2↓,
Hif1a↓,
FASN↓,
CRP↓,
IL6↓,
IL1β↓,
IFN-γ↓,
TNF-α↓,
Twist↓,
VEGF↓,
MMP2↓,
MMP9↓,

931- And,    Effect of Andrographis Paniculata Aqueous Extract on Hyperammonemia Induced Alteration of Oxidative and Nitrosative Stress Factors in the Liver, Spleen and Kidney of Rats
- in-vivo, NA, NA
*SOD↝, helped restore SOD, catalase, and GR levels
*Catalase↝,
*ROS↓, reducing oxidative stress
*MDA↓,
*NO↓,

3886- Api,    Neuroprotective effects of apigenin against inflammation, neuronal excitability and apoptosis in an induced pluripotent stem cell model of Alzheimer’s disease
- in-vitro, AD, NA
*Inflam↓, apigenin has potent anti-inflammatory properties with the ability to protect neurites and cell viability by promoting a global down-regulation of cytokine and nitric oxide (NO) release in inflammatory cells.
*neuroP↑, demonstrate the broad neuroprotective action of apigenin against AD pathogenesis in a human disease model.
*NO↓,
*Apoptosis↓, Apigenin reduces apoptosis in sporadic AD and control neurons

3665- ART/DHA,    Artemisinin B Improves Learning and Memory Impairment in AD Dementia Mice by Suppressing Neuroinflammation
- Review, AD, NA
*Inflam↓, artemisinin B from Artemisia annua Linn. has strong anti-inflammatory and immunological activities.
*NO↓, artemisinin B inhibited NO secretion from LPS-induced BV2 cells and significantly reduced the expression levels of the inflammatory cytokines IL-1β, IL-6 and TNF-α.
*IL1β↓,
*IL6↓,
*TNF-α↓,
*MyD88↓, accompanied by reduced gene expression levels of MyD88 and NF-κB as well as TLR4 and MyD88 protein levels
*NF-kB↓,
*TLR4↓,
*memory↑, artemisinin B improved spatial memory in dementia mice in the water maze and step-through tests

556- ART/DHA,    Artemisinins as a novel anti-cancer therapy: Targeting a global cancer pandemic through drug repurposing
- Review, NA, NA
IL6↓,
IL1↓, IL-1β
TNF-α↓,
TGF-β↓, TGF-β1
NF-kB↓,
MIP2↓,
PGE2↓,
NO↓,
Hif1a↓,
KDR/FLK-1↓,
VEGF↓,
MMP2↓,
TIMP2↑,
ITGB1↑,
NCAM↑,
p‑ATM↑,
p‑ATR↑,
p‑CHK1↑,
p‑Chk2↑,
Wnt/(β-catenin)↓,
PI3K↓,
Akt↓,
ERK↓, ERK1/2
cMyc↓,
mTOR↓,
survivin↓,
cMET↓,
EGFR↓,
cycD1/CCND1↓,
cycE1↓,
CDK4/6↓,
p16↑,
p27↑,
Apoptosis↑,
TumAuto↑,
Ferroptosis↑,
oncosis↑,
TumCCA↑, G0/G1 into M phase, G0/G1 into S phase, G1 and G2/M
ROS↑, ovarian cancer cell line model, artesunate induced oxidative stress, DNA double-strand breaks (DSBs) and downregulation of RAD51 foci
DNAdam↑,
RAD51↓,
HR↓,

1074- ART/DHA,    Artemisinin attenuates lipopolysaccharide-stimulated proinflammatory responses by inhibiting NF-κB pathway in microglia cells
- in-vitro, Nor, BV2
*TNF-α↓,
*IL6↓,
*MCP1↓,
*NO↓,
*iNOS↓,
*IκB↑,

1177- Ash,    Withaferin A downregulates COX-2/NF-κB signaling and modulates MMP-2/9 in experimental endometriosis
- in-vivo, EC, NA
TumVol↓,
MMP2↓,
MMP9↓,
NF-kB↓,
COX2↓,
NO↓,
IL1β↓,
IL6↓,

1146- AsP,    Potential use of nanoformulated ascorbyl palmitate as a promising anticancer agent: First comparative assessment between nano and free forms
- in-vivo, Nor, NA
TumCCA↑, G2/M phase
Apoptosis↑,
IL6↓,
STAT3↓,
angioG↓,
TumMeta↓,
VEGF↓,
MMP9↓,
SOD↑,
Catalase↑,
GSH↓,
MDA↓,
NO↓,
*BioAv↑, nano particles

5384- AsP,  MEL,    Synergistic Anticancer Effect of Melatonin and Ascorbyl Palmitate Nanoformulation: A Promising Combination for Cancer Therapy
- in-vivo, Var, NA
AntiCan↑, assess the anticancer effect of melatonin (MEL) and ascorbyl palmitate-loaded pluronic nanoparticles (APnp) combination on Ehrlich ascites carcinoma (EAC)-bearing mice.
TumCG↓, MEL alone showed a decrease in tumor growth by 48%, while in the case of using MEL combined with APnp, it displayed inhibition of tumor growth by 62%
Apoptosis↑, It also induced apoptosis and DNA damage.
DNAdam↑,
TumCCA↑, Besides, mediated cell cycle arrest.
IL6↓, IL-6/STAT3 pathway was inactivated to a greater extent after our combination treatment.
STAT3↓,
TumCP↓, antiproliferative effect of MEL and APnp via decreased expression of Ki-67
Ki-67↓,
TumCI↓, Our combination of MEL and APnp was able to inhibit cancer cell invasion and metastasis by decreasing the protein expression of MMP-9.
TumMeta↓,
MMP9↓,
eff↑, The synergy score was 21.06 ( > 10 indicates synergistic effect)
*Catalase↑, Administration of MEL alone or MEL+ APnp treated mice showed a significant and highly significant increase, respectively (P<0.05, P<0.01) in the antioxidant enzyme activities of CAT and SOD, and GSH.
*SOD↑,
*GSH↑,
*MDA↓, Figure 2 demonstrated a highly significant and extremely significant reduction, respectively (P<0.01, P<0.001) in the MDA and NO levels compared to the EAC control group.
*NO↓,
*antiOx↑, Figure 2 demonstrated a highly significant and extremely significant reduction, respectively (P<0.01, P<0.001) in the MDA and NO levels compared to the EAC control group.
*hepatoP↑, combined MEL and APnp- treated animals displayed a noteworthy amelioration for all examined organs when compared to the control EAC inoculated group, Figure 3.
*RenoP↑,

5419- ASTX,    Astaxanthin and other Nutrients from Haematococcus pluvialis—Multifunctional Applications
- Review, Nor, NA
*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.

4276- BA,    Baicalin Attenuates Oxygen–Glucose Deprivation/Reoxygenation–Induced Injury by Modulating the BDNF-TrkB/PI3K/Akt and MAPK/Erk1/2 Signaling Axes in Neuron–Astrocyte Cocultures
- in-vivo, Stroke, NA
*BDNF↑, has been indicated to protect neurons by promoting brain-derived neurotrophic factor (BDNF).
*neuroP↑, neuroprotective mechanisms of baicalin against oxygen–glucose deprivation/reoxygenation
*TrkB↑, baicalin significantly increased the expressions of TrkB, PI3K/AKT, and MAPK/ERK.
*PI3K↑,
*Akt↑,
*MAPK↑,
*ERK↑,
*NO↓, elevation of NO and MDA was significantly attenuated by BCL treatment.
*MDA↓,
*SOD↑, BCL treatment increased the expression level of SOD
*TNF-α↓, OGD/R treatment significantly increased the expression levels of TNF-α, IL-1β, and IL-6 (p < 0.01). Compared with that in the OGD/R group, BCL robustly reduced the release of inflammatory cytokines
*IL1β↓,
*IL6?,

1522- Ba,    Baicalein reduces lipopolysaccharide-induced inflammation via suppressing JAK/STATs activation and ROS production
- in-vitro, Nor, RAW264.7
*p‑STAT1↓, Baicalein significantly reduced the phosphorylation of STAT1 and STAT3 and the phosphorylation of JAK1 and JAK2
*p‑STAT3↓,
*p‑JAK1↓,
*p‑JAK2↓,
*iNOS↓, inhibited production of iNOS upon LPS-stimulation
*NO↓, inhibition of releases of NO and pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α, in a dose-dependent manner
*IL1β↓,
*IL6↓,
*TNF-α↓,
*ROS↓, baicalein reduced the LPS-induced accumulation of ROS

2626- Ba,    Molecular targets and therapeutic potential of baicalein: a review
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
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↓,

2749- BetA,    Anti-Inflammatory Activities of Betulinic Acid: A Review
- Review, Nor, NA
Inflam↓, betulinic acid as a promissory lead compound with anti-inflammatory activity
*NO↓, BA can inhibit the production of NO, mainly in macrophages cultures stimulated with bacterial lipopolysaccharide (LPS) and/or interferon gamma (IFN-ɣ)
*IL10↑, (BA) has a broad-spectrum anti-inflammatory activity, significantly increasing IL-10 production, decreasing ICAM-1, VCAM-1, and E-selectin expression and inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB),
*ICAM-1↓,
*VCAM-1↓,
*E-sel↓,
*NF-kB↓,
*IKKα↓, BA blocks the NF-κB signaling pathway by inhibiting IκB phosphorylation and d
*COX2↓, BA also inhibits cyclooxygenase-2 (COX-2) activity and, therefore, decrease prostaglandin E2 (PGE2) synthesis
*PGE2↓,
*IL1β↓, The production of critical pro-inflammatory cytokines, such as IL-1β, IL-6, IL-8, IL-12, and TNF, is also decreased by BA treatment
*IL6↓,
*IL8↓,
*IL12↓,
*TNF-α↑,
*HO-1↑, induction of HO-1 enzyme activity is associated with the anti-inflammatory effect of BA, since SnPP, an inhibitor of HO-1, promoted a partial reversal of BA’s effect on NF-κB activity,
*IL10↑, BA also increased the amount of IL-10, a well-known anti-inflammatory cytokine
*IL2↓, decreasing the production of pro-inflammatory cytokines, such as IL-2, IL-6, IL-17, and IFN-γ
*IL17↓,
*IFN-γ↓,
*SOD↑, BA decreased the production of the inflammatory mediators described above at the inflammation site and increased enzyme activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GRd) in the liver
*GPx↑,
*GSR↑,
*MDA↓, BA decreased malondialdehyde (MDA) levels, a key mediator of oxidative stress and widely used as a marker of free radical mediated lipid peroxidation injury, at the inflammation site
*MAPK↓, BA downregulates MAPK signaling pathways (ERK1/2, JNK, and p38) in the paw edema tissue, which, in part, explains the inhibition of cytokine production (IL-1β and TNF), COX-2 expression, and PGE2 production (Figure 3).

5656- BNL,    Role of borneol as enhancer in drug formulation: A review
- Review, Nor, NA - Review, Stroke, NA - Review, AD, NA
*eff↑, borneol has shown superior ability for anti-inflammatory and analgesic activities when coupled with other active ingredients from ancient times.
BBB↑, Given its ability to enhance cross-barrier permeation
ChemoSen↑, interest in borneol, for various purposes, including anti-inflammatory, analgesic, neuronal protection, permeability promotion, chemotherapy sensitization and borneol-modified nano-drug delivery system
*Inflam↓, borneol and its synthetic counterpart exhibit noteworthy anti-inflammatory properties by reducing inflammatory factors, namely NO, TNF-α, and IL-6
*NO↓,
*TNF-α↓,
*IL6↓,
*Bacteria↓, Borneol has shown exceptional anti-bacterial effect activity and has been coupled in TCM formulas for external use against bacteria growth
*eff↑, Studies indicated that the combined administration of edaravone and borneol (i.e. Edaravone Dexborneol) exhibited synergistic effects in the treatment of ischemic stroke
*Aβ↓, efficient prohibition of the accumulation of Aβ in the brain
*SOD↑, Borneol has been reported to exhibit exceptional potential in the augmentation of superoxide dismutase (SOD) activity
*neuroP↑, Both naturally occurring and artificially synthesized borneol exhibited neuroprotective properties
*EPR↑, The permeation-enhancing effects of natural borneol and synthetic borneol on various drug properties have been observed,
toxicity↓, Borneol is an ideal absorption enhancer with low toxicity, little stimulation to gastrointestinal mucosa and strong permeability
P-gp↓, The inhibition of P-gp expression has been observed as a potential mechanism for reversing multidrug resistance, with borneol implicated in this process
eff↑, Research findings indicated that natural borneol can substantially enhance the anticancer properties of paclitaxel and curcumin.
other↝, specifically, the incorporation of borneol has been associated with improvements in drug solubility, enhanced cellular uptake, reduced organ toxicity, and mitigation of multiple drug resistances.

3514- Bor,  CUR,    Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta
- in-vivo, AD, NA
*DNAdam↓, Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities.
*MDA↓,
*AChE↓,
*neuroP↑, BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure.
*ROS↓, BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed.
*NO↓, Synaptosomes treated with BA showed a significant reduction in MDA and NO levels

3507- Bor,    Boron inhibits apoptosis in hyperapoptosis condition: Acts by stabilizing the mitochondrial membrane and inhibiting matrix remodeling
*MMP↑, n the presence of boron, there was a significant and dose-dependent increase in MMP, which inhibited mitochondrial remodeling to the condensed state and hence the release of Cyt c and initiation of apoptosis.
*Cyt‑c↓, Boron inhibits the release of mitochondrial Cyt c and activation of Casp
*Apoptosis↓, Boron inhibits apoptosis.
*Casp3↓,
*NO↓, Nitric oxide (NO) and iNOS levels decrease in boron treated hyperapoptosis cultures.
*iNOS↓,

2776- Bos,    Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities
- Review, Var, NA
*5LO↓, Arthritis Human primary chondrocytes: 5-LOX↓, TNF-α↓, MMP3↓
*TNF-α↓,
*MMP3↓,
*COX1↓, COX-1↓, Leukotriene synthesis by 5-LOX↓
*COX2↓, Arthritis Human blood in vitro: COX-2↓, PGE2↓, TH1 cytokines↓, TH2 cytokines↑
*PGE2↓,
*Th2↑,
*Catalase↑, Ethanol-induced gastric ulcer: CAT↑, SOD↑, NO↑, PGE-2↑
*SOD↑,
*NO↑,
*PGE2↑,
*IL1β↓, inflammation Human PBMC, murine RAW264.7 macrophages: TNFα↓ IL-1β↓, IL-6↓, Th1 cytokines (IFNγ, IL-12)↓, Th2 cytokines (IL-4, IL-10)↑; iNOS↓, NO↓, phosphorylation of JNK and p38↓
*IL6↓,
*Th1 response↓,
*Th2↑,
*iNOS↓,
*NO↓,
*p‑JNK↓,
*p38↓,
GutMicro↑, colon carcinogenesis: gut microbiota; pAKT↓, GSK3β↓, cyclin D1↓
p‑Akt↓,
GSK‐3β↓,
cycD1/CCND1↓,
Akt↓, Prostate Ca: AKT and STAT3↓, stemness markers↓, androgen receptor↓, Sp1 promoter binding↓, p21(WAF1/CIP1)↑, cyclin D1↓, cyclin D2↓, DR5↑,CHOP↑, caspases-3/-8↑, PARP cleavage, NFκB↓, IKK↓, Bcl-2↓, Bcl-xL↓, caspase 3↑, DNA
STAT3↓,
CSCs↓,
AR↓,
P21↑,
DR5↑,
CHOP↑,
Casp3↑,
Casp8↑,
cl‑PARP↑,
DNAdam↑,
p‑RB1↓, Glioblastoma: pRB↓, FOXM1↓, PLK1↓, Aurora B/TOP2A pathway↓,CDC25C↓, pCDK1↓, cyclinB1↓, Aurora B↓, TOP2A↓, pERK-1/-2↓
FOXM1↓,
TOP2↓,
CDC25↓,
p‑CDK1↓,
p‑ERK↓,
MMP9↓, Pancreas Ca: Ki-67↓, CD31↓, COX-2↓, MMP-9↓, CXCR4↓, VEGF↓
VEGF↓,
angioG↓, Apoptosis↑, G2/M arrest, angiogenesis↓
ROS↑, ROS↑,
Cyt‑c↑, Leukemia : cytochrome c↑, AIF↑, SMAC/DIABLO↑, survivin↓, ICAD↓
AIF↑,
Diablo↑,
survivin↓,
ICAD↓,
ChemoSen↑, Breast Ca: enhancement in combination with doxorubicin
SOX9↓, SOX9↓
ER Stress↑, Cervix Ca : ER-stress protein GRP78↑, CHOP↑, calpain↑
GRP78/BiP↑,
cal2↓,
AMPK↓, Breast Ca: AMPK/mTOR signaling↓
mTOR↓,
ROS↓, Boswellia extracts and its phytochemicals reduced oxidative stress (in terms of inhibition of ROS and RNS generation)

6557- BSB,    Alpha-bisabolol protects against neonatal asthma by suppressing airway inflammatory signaling
- in-vivo, Nor, NA
*ROS↓, AB significantly decreased mucous gland hypertrophy, eosinophil infiltration, and oxidative stress marker levels in the allergic airway inflammation-induced AB-pretreated rats.
*Inflam↓, AB pretreatment significantly reduced the levels of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-8, IL-17, monocyte chemoattractant protein-1, C-X-C chemokine receptor type 4 (CXCR4), and thymic stromal lymphopoietin, which were i
*IL1β↓,
*IL6↓,
*IL8↓,
*IL17↓,
*CXCR4↓,
*COX2↓, transcription of cyclooxygenase-2, tumor necrosis factor-α, CXCR4, toll-like receptor 4, Eotaxin-1, and regulated upon activation normal T cell expressed and secreted were significantly suppressed in allergic airway inflammation-induced AB-pretreated
*TLR4↓,
*NO↓, NO, PCO, MDA, and XO, all of these oxidative stress parameters were significantly attenuated in AB-treated allergic airway inflammation-induced rat pups
*MDA↓,
*XO↓,

4263- CA,    Neuroprotective Effects of Carnosic Acid: Insight into Its Mechanisms of Action
- Review, AD, NA
*neuroP↑, neuroprotective effect of CA on neuronal cells subjected to ischemia/hypoxia injury via the scavenging or reduction of ROS (reactive oxygen species) and NO (nitric oxide) and inhibition of COX-2 and MAPK pathways
*ROS↓,
*NO↓,
*COX2↓,
*MAPK↓,
*NRF2↑, CA is known to activate the Keap1/Nrf2 pathway, thereby resulting in the production of cytoprotective proteins.
*GSH↑, activation of GSH metabolism
*HO-1↑, activation of Nrf2 target genes, including heme oxygenase 1 (HO-1) and thioredoxin reductase 1 (TXNRD1)
*5HT↑, Observations of increased serotonin and BDNF suggest that CA may represent a novel therapeutic avenue for depressive behaviors that should be further explored.
*BDNF↑, 10 μM CA results in a 1.5-fold increase in levels of BDNF
*PI3K↑, CA has been shown to mediate the activation of the PI3K/Akt/NF-κB pathway
*Akt↑,
*NF-kB↑,
*BBB↑, CA was shown to ameliorate brain edema and blood-brain barrier (BBB) disruption
*SIRT1↑, CA was also shown to increase SIRT1
*memory↑, CA was shown to significantly improve short-term and spatial memory attributes in rat models of AD
*Aβ↓, CA also delayed the deposition of Aβ and protected cells against Aβ-induced cholinergic and mitochondrial dysfunction in a Caenorhabditis elegans model of AD
*NLRP3↓, CA also inhibits the nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome, which plays a critical role in the pathogenesis of neurodegenerative disorders, including AD and PD and COVID-19

5927- CAR,    Neuroprotective Potential and Underlying Pharmacological Mechanism of Carvacrol for Alzheimer’s and Parkinson’s Diseases
- Review, AD, NA - Review, Park, NA
*memory↑, Carvacrol enhances memory and cognition by modulating the effects of oxidative stress, inflammation, and Aβ25-35-induced neurotoxicity in AD
*cognitive↑,
*ROS↓, reduces the production of reactive oxygen species and proinflammatory cytokine levels in PD
*Inflam↓,
*motorD↑, improves motor functions
*toxicity↓, in general, it is potentially safe for consumption
*TRPV3↑, Carvacrol is a potent agonist of transient receptor potential vanilloid 3 (TRPV3)
*other↓, mitigating oxidative stress (OS)/ADP-ribose (ADPR)-induced TRPM2 and GSK1016790A (GSK)-mediated TRPV4 activations
*antiOx↑, Essential oils, high in carvacrol, have powerful antioxidant properties [85-88] similar to vitamin E, ascorbic acid, and butyl hydroxyl toluene
*LDL↓, Low-density lipoprotein (LDL) is inhibited by carvacrol in vitro and mediates LDL oxidation within an incubation period of 12 h
*COX2↓, suppressing the expression level of cyclooxygenase-2 (COX-2),
*PPARα↑, triggering the peroxisome proliferator-activated receptors (PPAR) α and γ
*NO↓, inhibiting NO production
*AChE↓, Carvacrol's acetylcholinesterase inhibitory action is 10 times higher than thymol's, even though the two compounds have a relatively similar structure
*eff↑, carvacrol nanoemulsion treatment has shown more notable effects compared to carvacrol oil.
*SOD↑, increases superoxide dismutase (SOD) and catalase (CAT) activity
*Catalase↑,
*neuroP↑, neuroprotective effects of carvacrol against cognitive impairments and its potential in AD are shown in Fig. (2)
*BioAv↝, In rabbits, 1.5 g of orally administered carvacrol is progressively absorbed from the intestines, with approximately 30% of the whole dose remaining in the gastrointestinal system and 25% eliminated via urine after 22 h of administratio
*BBB↑, carvacrol in the brain tissues as it easily crosses the blood-brain barrier owing to its low molecular weight (150.2 g/mol) and higher lipophilicity
*BioAv↑, liposomal encapsulation [136], and solid lipid nanoparticles [137], were developed and found bioavailable on oral administration. These formulations exhibit improved solubility, stability, and bioavailability and enhance drug accumulation in the tiss

5932- CAR,    Carvacrol attenuates mucosal barrier impairment and tumorigenesis by regulating gut microbiome
- in-vivo, IBD, NA - in-vivo, Park, NA
*GutMicro↑, Carvacrol can regulate the gut microbiota. bundance of specific microbiota, such as Lactobacillus, Escherichia coli/Shigella, and Lachnoclostridium.
Risk↓, Carvacrol inhibits the development of colitis-associated colorectal cancer.
*Inflam↓, nti-inflammatory and antioxidant traits,
*antiOx↓,
*ZO-1↑, carvacrol significantly restored colonic length (p < 0.01) and re-established key tight junction proteins like ZO-1.
*iNOS↓, downregulated mRNA levels of inflammatory mediators such as iNOS and IL-6.
*IL6↓,
*NO↓, carvacrol has been shown to suppress nitric oxide and prostaglandin E2 production
*PGE2↓,
*memory↑, carvacrol improves memory deficits in Parkinson’s disease models
*TLR4↓, anti-inflammatory effects of carvacrol by inhibiting the TLR4/NF-κB signaling pathway
*NF-kB↓,
*IBI↑, Carvacrol improves intestinal barrier function
*CLDN3↑, expression levels of ZO-1, Claudin3, Claudin1, Occludin, and Mucin were significantly increased in the carvacrol group compared to the DSS group
*CLDN1↑,
*MUC1↑,
*OCLN↑,
*iNOS↑, carvacrol significantly inhibited the mRNA expression levels of iNOS, COX-2, Interferon-γ, IL-1β, and IL-6 in the intestinal tracts of colitis mice
*COX2↓,
*IFN-γ↓,
IL1β↓,
ADAM10?,

3871- Carno,    Unveiling the Hidden Therapeutic Potential of Carnosine, a Molecule with a Multimodal Mechanism of Action: A Position Paper
- Review, NA, NA
*ROS↓, detoxification of reactive oxygen and nitrogen species, the down-regulation of the production of pro-inflammatory mediators,
*NO↓,
*Inflam↓,

3872- Carno,    Carnosine Protects Macrophages against the Toxicity of Aβ1-42 Oligomers by Decreasing Oxidative Stress
- in-vitro, AD, NA
*antiOx↑, well-known antioxidant, anti-inflammatory, and anti-aggregation activities, and it may be useful for treatment of neurodegenerative disorders such as Alzheimer’s disease (AD)
*Inflam↓,
*Aβ↓,
*neuroP↑,
*ROS↓, by decreasing oxidative stress as measured by levels of intracellular nitric oxide (NO)/reactive oxygen species (ROS) and production of peroxynitrite
*NO↓,

6660- Cen,    Hepatoprotective effect of Centella asiatica 50% ethanol extract against acetaminophen-induced acute liver injury in BALB/c mice
*hepatoP↑, biomarkers of liver injury, were significantly increased by APAP and dose-dependently decreased by CA-HE50
*NO↓, inhibiting the release of nitric oxide from these cells;
*lipid-P↓, CA-HE50 inhibits lipid peroxidation in the liver
*IL1β↓, xpression of IL-1β was significantly suppressed by all doses of CA-HE50
*ALAT↓, CA-HE50 pre-treatment dose-dependently decreased the APAP-induced increase in levels of serum ALT, AST, and LDH levels, indicating that CA-HE50 has a protective effect against fulminant liver injury.
*AST↓,
*LDH↓,
GSH↑, GSH depletion and MDA overproduction caused by APAP were reversed by CA-HE50 treatment.
MDA↓,

6649- Cen,    Centella asiatica Extract Improves Behavioral Deficits in a Mouse Model of Alzheimer's Disease: Investigation of a Possible Mechanism of Action
- in-vivo, AD, NA
*eff↑, Orally administered GKW attenuated β-amyloid-associated behavioral abnormalities in these mice.
*memory↑, CA extract markedly improved learning and memory of wild-type rats
*NO↓, GKW inhibited NO production induced by Aβ but did not influence LPS-induced NO levels in these cells.
*cognitive↑, Other potential mechanisms by which GKW may have improved cognitive function in the Tg2576 mice were also investigated
*AChE∅, No direct inhibitory effect of GKW (2.5 to 250 μg/mL) on cholinesterase activity in vitro was observed

6018- CGA,    Chlorogenic acid: a review on its mechanisms of anti-inflammation, disease treatment, and related delivery systems
- Review, Var, NA - Review, RCC, NA
*BioAv↓, Nevertheless, the inherent low bioavailability of chlorogenic acid poses challenges in practical deployments.
*Inflam↓, chlorogenic acid predominantly impedes the synthesis and secretion of inflammatory mediators such as TNF-α, NO, COX-2, and PGE2.
*TNF-α↓,
*NO↓,
*COX2↓,
*PGE2↓,
*NF-kB↓, Inhibition of NF-κB signaling pathway
*IL6↓, downregulates inflammatory mediators including IL-6, TNF-α, IL-1β, and TLR2 by hindering the phosphorylation of NF-κB pathway proteins,
*IL1β↓,
*TLR2↓,
*MAPK↓, Inhibition of MAPK signaling pathway
*NRF2↓, Activation of the Nrf2 signaling pathway
*HO-1↑, concomitant upregulation of HO-1 and NQO-1
*NQO1↑,
*cardioP↑, its cardioprotective attributes are further elucidated through modulating pertinent signaling pathways
*neuroP↑, This neuroprotection appears to correlate with an upregulation in SOD2 expression facilitated by chlorogenic acid
*SOD↑,
*GSH↑, compound bolsters SOD activity, elevates GSH concentrations, curtails ROS and LDH production, reduces MDA accumulation, and ameliorates cerebral ischemia-reperfusion (CI/R) injury sequels
*ROS↓,
*LDH↓,
*MDA↓,
*cognitive↑, Chlorogenic acid ameliorates such cognitive deficits, a process conceivably attributed to its inhibitory action on NF-κB and IL-6 within frontal brain structures (
*eff↑, One pivotal investigation showcased that bovine serum albumin (BSA)-facilitated chlorogenic acid silver nanoparticles (AgNPs-CGA-BSA) exude substantial antioxidant and anti-neoplastic properties across in vivo and in vitro matrices.

2794- CHr,    An updated review on the versatile role of chrysin in neurological diseases: Chemistry, pharmacology, and drug delivery approaches
- Review, Park, NA - Review, Stroke, NA
*neuroP↑, chrysin has protective effects against neurological conditions by modulating oxidative stress, inflammation, and apoptosis in animal models.
*ROS↓,
*Inflam↓,
*Apoptosis↓,
*IL1β↓, attenuated IL-1β and TNF-α, COX-2, iNOS, and NF-kB expression, activated JNK
*TNF-α↓,
*COX2↓,
*iNOS↓,
*NF-kB↓,
*JNK↓,
*HDAC↓, alleviated histone deacetylase (HDCA) activity, GSK-3β levels, IFNγ, IL-17,
*GSK‐3β↓,
*IFN-γ↓,
*IL17↓,
*GSH↑, increased GSH levels
*NRF2↑, Park's: Increased Nrf2, modulated HO-1, SOD, CAT, decreased MDA, inhibited NF-κB and iNOS
*HO-1↑, upregulated expression of hallmark antioxidant enzymes, including HO-1, SOD, and CAT; and decreased levels of MDA
*SOD↑,
*MDA↓,
*NO↓, Attenuated NO, increased GPx
*GPx↑,
*TBARS↓, decreased levels of TBARS, AChE, restored activities of GR, GSH, SOD, CAT and Vitamin C
*AChE↓,
*GR↑,
*Catalase↑,
*VitC↑,
*memory↑, attenuated memory impairment
*lipid-P↓, attenuated lipid peroxidation
*ROS↓, attenuated ROS

6297- Cro,    Crocetin Exerts Its Anti-inflammatory Property in LPS-Induced RAW264.7 Cells Potentially via Modulation on the Crosstalk between MEK1/JNK/NF-κB/iNOS Pathway and Nrf2/HO-1 Pathway
- in-vitro, Nor, RAW264.7
*NO↓, crocetin dose-dependently inhibited LPS-induced nitric oxide production and inducible nitric oxide synthase (iNOS) expression in RAW264.7 cells.
*iNOS↓,
*Inflam↓, anti-inflammatory property by inhibiting the MEK1/JNK/NF-κB/iNOS pathway and activating the Nrf2/HO-1 pathway.
*MEK↓,
JNK↓,
NF-kB↓, Crocetin Inhibits the Activation of the Nuclear Factor kappaB (NF-κB)
NRF2↑,
HO-1↑,
hepatoP↑, Gardenia jasminoides can possess various pharmacological activities in hepatochemoprevention [4, 5], neuroprotection [6], anti-inflammatory regulation
neuroP↑,

6529- CRV,    D-Carvone Attenuates CCl4-Induced Liver Fibrosis in Rats by Inhibiting Oxidative Stress and TGF-ß 1/SMAD3 Signaling Pathway
- in-vivo, Nor, NA
*ALAT↓, D-carvone significantly enhanced liver functions (ALT, AST), oxidant/antioxidant status (MDA, SOD, GSH, total antioxidant capacity; TAC), as well as histopathological changes.
*AST↓, administration with D-carvone (50 mg/kg, bw) significantly reduced serum ALT and AST to 54.8% and 51% compared to the CCl4 model group, respectively
*MDA↓, decreased the MDA levels to 50.7%, while it restored the depleted GSH and SOD levels to 233% and 221.5%, respectively
*SOD↑,
*GSH↑,
*TAC↑,
*eff↑, D-carvone effectively attenuated the progression of liver fibrosis, evident by the decreased collagen deposition and fibrosis score by Masson trichrome staining (MT) and α-SMA protein expression
*TGF-β1↓, significant downregulation of the pro-fibrogenic markers TGF-β1 and SMAD3 and upregulation of MMP9.
*SMAD3↓,
*MMP9↑,
*NRF2↑, D-carvone promotes the Nrf2 signaling pathway which might contribute to the antioxidative activity of D-carvone
*antiOx↑,
*hepatoP↑,
*Inflam↓, D-carvone administration appreciably reduced the inflammatory cells’ infiltration and pro-inflammatory modulators release provoked by liver injury
*NF-kB↓, D-carvone include downregulation of NF-κB
*NO↓, D-carvone has been reported to diminish the excessively produced NO by macrophages and Kupffer cells in the injured liver
*cAMP↑, carvone has been found to activate the cyclic adenosine monophosphate (cAMP) signaling pathway
*ROS↓, by Inhibiting Oxidative Stress

2308- CUR,    Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells
- in-vitro, Liver, HepG2
GlucoseCon↓, Curcumin obviated the hyperglycemia-induced modulations like elevated glucose consumption, lactate production, and extracellular acidification, and diminished nitric oxide and reactive oxygen species (ROS) production
lactateProd↓,
ECAR↓,
NO↓,
ROS↑, Curcumin favors the ROS production in HepG2 cells in normal as well as hyperglycemic conditions. ROS production was detected in cancer cells treated with curcumin, or doxorubicin, or their combinations in NG or HG medium for 24 h
HK2↓, HKII, PFK1, GAPDH, PKM2, LDH-A, IDH3A, and FASN. Metabolite transporters and receptors (GLUT-1, MCT-1, MCT-4, and HCAR-1) were also found upregulated in high glucose exposed HepG2 cells. Curcumin inhibited the elevated expression of these enzymes, tr
PFK1↓,
GAPDH↓,
PKM2↓,
LDHA↓,
FASN↓,
GLUT1↓, Curcumin treatment was able to significantly decrease the expression of GLUT1, HKII, and HIF-1α in HepG2 cells either incubated in NG or HG medium.
MCT1↓,
MCT4↓,
HCAR1↓,
SDH↑, Curcumin also uplifted the SDH expression, which was inhibited in high glucose condition
ChemoSen↑, Curcumin Prevents High Glucose-Induced Chemoresistance
ROS↑, Treatment of cells with doxorubicin in presence of curcumin was found to cooperatively augment the ROS level in cells of both NG and HG groups.
BioAv↑, Curcumin Favors Drug Accumulation in Cancer Cells
P53↑, An increased expression of p53 in curcumin-treated cells can be suggestive of susceptibility towards cytotoxic action of anticancer drugs
NF-kB↓, curcumin has therapeutic benefits in hyperglycemia-associated pathological manifestations and through NF-κB inhibition
pH↑, Curcumin treatment was found to resist the lowering of pH of culture supernatant both in NG as well in HG medium.

2818- CUR,    Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways
- Review, AD, NA
*neuroP↑, Curcumin's protective functions against neural cell degeneration due to mitochondrial dysfunction and consequent events such as oxidative stress, inflammation, and apoptosis in neural cells have been documented
*ROS↓, studies show that curcumin exerts neuroprotective effects on oxidative stress.
*Inflam↓,
*Apoptosis↓,
*cognitive↑, cognitive performance to receive the title of neuroprotective
*cardioP↑, Studies have shown that curcumin can induce cell regeneration and defense in multiple organs such as the brain, cardiovascular system,
other↑, It has been shown that chronic use of curcumin in patients with neurodegenerative disorder can cause gray matter volume increase
*COX2↓, Curcumin also decreased the brain protein levels and activity of cyclooxygenase 2 (COX-2)
*IL1β↓, inhibition of IL-1β and TNF-α production, and enhancement of Nf-Kβ inhibition
*TNF-α↓,
NF-kB↓,
*PGE2↓, hronic curcumin therapy has shown a significant decrease in lipopolysaccharide (LPS)-induced elevation of brain prostaglandin E2 (PGE2) synthesis in rats
*iNOS↓, curcumin pretreatment decreased NOS activity in the ischemic rat model
*NO↓, curcumin has been shown to decrease NOS expression and NO production in rat brain tissue
*IL2↓, IL-2 is a cytokine that is anti-inflammatory. Numerous studies have shown that curcumin increases the secretion of IL-2
*IL4↓, curcumin reduced levels of IL-4
*IL6↓, Numerous studies have shown that curcumin in neurodegenerative events attenuates IL-6 production
*INF-γ↓, curcumin reduced the production of INF-γ, as pro-inflammatory cytokine
*GSK‐3β↓, Furthermore, previous findings have confirmed that inhibition of GSK-3β or CREB activation by curcumin has reduced the production of pro-inflammatory mediators under different conditions
*STAT↓, Inhibition of GSK-3β by curcumin has been found to result in reduced STAT activation
*GSH↑, chronic curcumin therapy increased glutathione levels in primary cultivated rat cerebral cortical cells
*MDA↓, multiple doses of 5, 10, 40 and 60 mg/kg) in rodents will inhibit neurodegenerative agent malicious effects, and reduce the amount of MDA and lipid peroxidation in brain tissue
*lipid-P↓,
*SOD↑, Curcumin induces increased production of SOD, glutathione peroxidase (GPx), CAT, and glutathione reductase (GR) activating antioxidant defenses
*GPx↑,
*Catalase↑,
*GSR↓,
*LDH↓, Curcumin decreased lactate dehydrogenase, lipoid peroxidation, ROS, H2O2 and inhibited Caspase 3 and 9
*H2O2↓,
*Casp3↓,
*Casp9↓,
*NRF2↑, ncreased mitochondrial uncoupling protein 2 and increased mitochondrial biogenesis. Nuclear factor-erythroid 2-related factor 2 (Nrf2)
*AIF↓, Curcumin treatment decreased the number of AIF positive nuclei 24 h after treatment in the hippocampus,
*ATP↑, curcumin in hippocampal cells induced an increase in mitochondrial mass leading to increased production of ATP with major improvements in mitochondrial efficiency

1792- CUR,  LEC,    Chondroprotective effect of curcumin and lecithin complex in human chondrocytes stimulated by IL-1β via an anti-inflammatory mechanism
- in-vitro, Arthritis, RAW264.7 - NA, NA, HCC-38
*Inflam↓, curcumin is well known to regulate anti-inflammatory effects, primarily through the deactivation of NF-κB
*NF-kB↓,
*iNOS↓, 10 and 20 μM, complex also suppressed iNOS and COX-2 mRNA expression and inhibited NO and PGE2 production
*COX2↓,
*NO↓,
*PGE2↓,
*MMPs↑, 10 and 20 μM of the complex (Fig. 2A, B, and C). IL-1β noticeably upregulated the production of MMP-1, 2, 3, 9, and 13 and TIMP-1 compared to the control group
*TIMP1↑,
*BioEnh↑, In this study, the complex of curcumin and lecithin enhanced bioavailability of curcumin resulting in chondroprotective effect at relatively lower concentrations.

1418- CUR,    Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis
- Review, Arthritis, NA
*COX2↓, Curcumin downregulates the cyclooxygenase-2 (COX-2) pathway, reducing the production of prostaglandins associated with inflammation
*Inflam↓,
*5LO↓, directly inhibits lipoxygenase (LOX)
*NO↓,
*NF-kB↓,
*TNF-α↓,
*IL1↓,
*IL2↑,
*IL6↓,
*IL8↓,
*IL12↓,
*MCP1↓,
*PGE2↓,
*MMP2↓,
*MMP3↓,
*MMP9↓,
*NLRP3↓,
*ROS↓, arthritis(basically normal cell)

6692- DFC,    Diclofenac Inhibits Tumor Growth in a Murine Model of Pancreatic Cancer by Modulation of VEGF Levels and Arginase Activity
- in-vivo, PC, Panc02
TumW↓, We found that diclofenac treatment (30 mg/kg/bw for 11 days) of mice inoculated with PANC02 cells, reduced the tumor weight by 60%, correlating with increased apoptosis of tumor cells.
Apoptosis↑,
VEGF↓, diclofenac drastically decreased tumor vascularization by downregulating VEGF in the tumor and in abdominal cavity fluid.
COX2↓, in contrast to other COX-2 inhibitors, diclofenac increased arginase activity/arginase 1 protein content in tumor stroma cells, peritoneal macrophages and white blood cells by 2.4, 4.8 and 2 fold, respectively.
ARG1/2↑, Diclofenac increases arginase activity in pancreatic tumors and in peritoneal macrophages, but not in bone marrow-CD 115 positive and CD 115 negative cells
TumCG↓, Diclofenac inhibits tumor growth in an orthotopic model of pancreatic cancer in mice
angioG↓, Tumors from diclofenac treated animals were very pale (Fig 1A), suggesting that the treatment caused an antiangiogenic effect.
ARG↓, subsequent arginine depletion and decrease in NO levels, both in serum and peritoneal cavity, adds to tumor growth inhibition by malnourishment and poor vasculature development.
NO↓,

6328- DRE,    Hydroalcoholic extract of Taraxacum officinale induces apoptosis and autophagy in 4T1 breast cancer cells
- in-vitro, BC, 4T1
TumCG↓, HADE inhibited cell growth and proliferation in a dose- and time-dependent manner.
TumCP↓,
Apoptosis↑, The HADE induced 4T1 breast cancer cell death via apoptosis and autophagy.
TumAuto↑,
DNAdam↑, DNA fragmentation was improved as the concentration of HADE increased.
BAX↑, The Bax, Bax/Bcl-2 ratio, p53, Beclin-1 and Atg-7 over-expression as well as Bcl-2 down-regulation were also evident in treated cancer cells.
Bax:Bcl2↑,
P53↑,
Beclin-1↑,
ATG7↑,
Bcl-2↓,
NO↓, The NO production in 4T1 cells was significantly (p < 0.05) decreased in all three concentrations of HADE after 24 hr incubation in a dose-dependent manner (

6317- DRE,    The efficacy of dandelion root extract in inducing apoptosis in drug-resistant human melanoma cells
- in-vitro, Melanoma, A375
Apoptosis↑, we show that dandelion root extract (DRE) specifically and effectively induces apoptosis in human melanoma cells without inducing toxicity in noncancerous cells.
selectivity↑,
Casp8↑, DRE-induced apoptosis activates caspase-8 in A375 cells early on, demonstrating employment of an extrinsic apoptotic pathway to kill A375 cells
mt-ROS↑, Reactive Oxygen Species (ROS) generated from DRE-treated isolated mitochondria indicates that natural compounds in DRE can also directly target mitochondria.
eff↑, Interestingly, the relatively resistant G361 human melanoma cell line responded to DRE when combined with the metabolism interfering antitype II diabetic drug metformin.
*toxicity↓, without toxicity to healthy cells. This triterpene is regarded as cytostatic and not cytotoxic.
Diff↑, Taraxacum Officinale was an effective inducer of differentiation in mouse melanoma cells.
TumCP↓, up-regulated melanogenesis and decreased cell proliferation in mouse melanoma [7].
chemoPv↑, taraxasterol (a triterpenoid), is a worthy chemopreventative agent
*ROS↓, ethanolic Taraxacum Officinale extracts and derivative forms thereof reduce levels of reactive oxygen species (ROS) and nitric oxide production (NO) and inhibit COX-2 expression or its antioxidant activity,
*NO↓, Dandelion flower extracts (DFE) were tested on RAW264.7 cells (mouse macrophages) and exhibited inhibition of NO production in these noncancerous cells.
*COX2↓,
*RNS↓, The inhibition of reactive nitrogen species (RNS) as well as ROS by DFE was attributed to its phenolic components
TumCI↓, Inhibition of cell invasion was corroborated by reduced matrix metalloproteinase activity of MMP-2 and -9, as well as reduced phosphorylation levels of src and FAK [2]
MMP2↓,
MMP9↓,
p‑Src↓,
p‑FAK↓,

20- EGCG,    Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer
- in-vivo, Liver, NA - in-vivo, Tong, NA
HH↓,
Gli1↓,
Smo↓,
TNF-α↓,
COX2↓, EGCG inhibits cyclooxygenase-2 without affecting COX-1 expression at both the mRNA and protein levels, in androgen-sensitive LNCaP and androgen-insensitive PC-3
*antiOx↑, EGCG is a well-known antioxidant and it scavenges most free radicals, such as ROS and RNS
Hif1a↓,
NF-kB↓,
VEGF↓,
STAT3↓,
Bcl-2↓,
P53↑, EGCG activates p53 in human prostate cancer cells
Akt↓,
p‑Akt↓,
p‑mTOR↓,
EGFR↓,
AP-1↓,
BAX↑,
ROS↑, apoptosis was convoyed by ROS production and caspase-3 cleavage
Casp3↑,
Apoptosis↑,
NRF2↑, pancreatic cancer cells via inducing cellular reactive oxygen species (ROS) accumulation and activating Nrf2 signaling
*H2O2↓, EGCG plays a role in the inhibition of H2O2 and NO production in human skin [10].
*NO↓, EGCG plays a role in the inhibition of H2O2 and NO production in human skin [10].
*SOD↑, fig 2
*Catalase↑, fig 2
*GPx↑, fig 2
*ROS↓, fig 2

6780- EGCG,    The pharmacological activity of epigallocatechin-3-gallate (EGCG) on Alzheimer's disease animal model: A systematic review
- Review, AD, NA
*neuroP↑, Regulation of α-, β-, γ-secretase activity, inhibition of tau phosphorylation, anti-oxidation, anti-inflammation, anti-apoptosis, and inhibition of AchE activity are reported as the main neuroprotective mechanisms.
*tau↓,
*antiOx↑,
*Inflam↓,
*Apoptosis↓,
*AChE↓,
*TNF-α↓, Inhibiting TNF-α/JNK pathway
*JNK↓,
*NGF↑, Increasing the level of NGF. EGCG (2 mg/kg) mouse
*SOD↑, figure 7
*GPx↑, EGCG enhanced the activity of T-SOD and GSH-Px and reduced MDA content in the hippocampus.
*MDA↓,
*NO↓,
*ROS↓,
*iNOS↓,
*COX2↓, anti apoptosis
*BAX↓, EGCG prevented LPS-induced elevation of GFAP, iNOS, and COX-2.
*CHOP↓,
*GRP78/BiP↓,
*Bcl-2↑,
*Dose↑, The highest safe dose for more than a month of treatment allowed by FDA is 800 mg of EGCG daily with food.
*BioAv↑, In preclinical and phase I clinical trials, it has been shown that bioavailability of EGCG is increased when it is consumed on a fasting basis.
*hepatoP↓, However, the rate of hepatotoxicity is also increased

6784- EGCG,    Dietary (−)-Epigallocatechin Gallate (EGCG): State-of-the-Art Advances in Bioactivities, Bioavailability Enhancement Strategies, and Applications in Nutrition and Health
- Review, Nor, NA
*antiOx↑, bioactivities of EGCG, including its antioxidant, anti-inflammatory, anticancer, cardiovascular protective, metabolic regulatory, neuroprotective, gut microbiota-modulating, and antimicrobial properties.
*Inflam↓,
*AntiCan↑,
*cardioP↑,
*neuroP↑,
*GutMicro↑,
*AntiBio↑,
*ROS↓, Figure 1, anti inflammatory
*TNF-α↓,
*IL6↓,
TumCP↓,
*LDL↓, cardioprotective
*NO↓,
*Obesity↓, Metabolic syndrome
*p‑tau↓, nervous system
*Aβ↓,
*NRF2↑, , EGCG has been shown to activate the Keap1/P62/Nrf2 signaling pathway,
*SOD↑, upregulation of endogenous antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, indirectly diminishing the levels of intracellular oxygen free radicals
*Catalase↑,
*GPx↑,
*NLRP3↓, EGCG also restores autophagy levels, suppresses the activation of the NLRP3 inflammasome by inhibiting the mammalian target of rapamycin signaling pathway
*mTOR↓,
TumCCA↑, Cancer: induce cell cycle arrest and inhibit tumor cell proliferation
NRF2↓, EGCG inhibits CCL5-stimulated lung cancer cell proliferation by down-regulating Nrf2 expression
Apoptosis↑, Inducing Apoptosis in Cancer Cells
SIRT1↓, EGCG activates the mitochondrial apoptotic pathway by downregulating SIRT1 expression to modulate the SIRT1-p53 axis
miR-25-5p↓, In breast cancer, EGCG induces apoptosis by inhibiting miR-25 expression and elevating PARP, pre-caspase-3 and pre-caspase-9 protein levels
PARP↑,
Casp3↑,
Casp9↑,
ER Stress↑, in multiple myeloma, EGCG promotes apoptosis by activating the endoplasmic reticulum stress pathway
TumAuto↑, EGCG induces autophagic cell death in breast cancer cells by retaining YAP1 in the cytoplasm and promoting the assembly of the CHMP2B-VPS4B complex
EMT↓, EGCG has been demonstrated to inhibit EMT, invasion, and migration by blocking the TGFβ/Smad signaling pathway
TumCI↓,
TumCMig↓,
TGF-β↓,
Smad1↓,
STAT3↓, EGCG can directly bind to STAT3, reducing nuclear localization and inhibiting the transcription of PLXNC1.
VEGF↓, widely believed that EGCG can block this process by reducing the expression of vascular endothelial growth factor, a key factor in angiogenesis,
angioG↓, The inhibition of angiogenic mimicry by EGCG through the Twist/VE-calmodulin/AKT pathway has also been demonstrated in prostate cancer cells
Imm↑, Acting as an Immunomodulator
EGFR↓, EGCG possesses the ability to interact with EGFR and inhibit activity, strengthening the anticancer evidence for EGCG
*GutMicro↑, EGCG can regulate the balance of gut flora. For example, EGCG can inhibit the growth of harmful bacteria such as Escherichia coli and Salmonella, while promoting the proliferation of probiotics like Bifidobacterium and Lactobacillus
*Bacteria↓, Antibacterial and Antiviral Properties of EGCG
*AntiViral↑,
*BioAv↓, EGCG, its low bioavailability in the human body limits clinical efficacy.
*BioAv↑, Nanotechnology strategy of EGCG.
*eff↑, Co-encapsulation assay of EGCG with quercetin shows that the two synergistically enhanced the antioxidant capacity of EGCG
*BioAv↑, Combining EGCG with resveratrol increases its solubility and significantly improves its absorption in the small intestine.
eff↑, combination of EGCG and curcumin inhibits the activity of metabolic enzymes, reduces the rate of metabolism in the liver and enhances its antitumor efficacy
ChemoSen↑, synergistic effects of EGCG combined with chemotherapeutic agents such as 5-fluorouracil, celecoxib, cisplatin, and tamoxifen have also been reported
*toxicity↝, The European Food Safety Authority notes in scientific opinion that daily oral doses of 800 mg or higher of EGCG represent a common starting point for observed cases of liver injury

1974- EGCG,    Protective Effect of Epigallocatechin-3-Gallate in Hydrogen Peroxide-Induced Oxidative Damage in Chicken Lymphocytes
- in-vitro, Nor, NA
*ROS↓, suppressed the increase in intracellular reactive oxygen species (ROS), nitric oxide (NO),
*NO↓,
*MMP↑, preincubation of the cells with EGCG increased mitochondrial membrane potential (MMP) and reduced calcium ion ([Ca2+]i) load.
*i-Ca+2↓, EGCC Increased Mitochondrial Membrane Potential and Decreased [Ca2+]i
*HO-1↑, expression of SOD, Heme oxygenase-1 (HO-1), Catalase (CAT), GSH-PX, nuclear factor erythroid 2-related factor 2 (Nrf2), and thioredoxin-1 (Trx-1).
*Catalase↑,
*NRF2↑,
*Trx1↑,
*antiOx↑, EGCC Increased Antioxidant Capacity
*SOD↑, EGCC Decreased ROS and Increased SOD Generation
*Apoptosis↓,

6819- EMD,    Recent advances in the therapeutic potential of emodin for human health
- Review, Nor, NA
AntiCan↑, It has therapeutic effects in cancer, diabetes, neurodegenerative diseases or chronic inflammatory diseases.
*AntiDiabetic↑, anticancer, neuroprotective, antidiabetic, antioxidant and anti-inflammatory.
*neuroP↑,
*Inflam↓,
*antiOx↑,
*BioAv↓, Because its bioavailability is low, there are limitations in clinical therapeutic use.
*BioAv↑, combined administration of emodin and piperine has been observed to clinically improve emodin pharmacokinetics, increasing 221 % of the area under the curve (AUC), 258 % the maximum concentration (Cmax), and decreasing 230 % the clearance related to
*SOD↑, fig 2 antioxidant
*GPx↑,
*GSH↑,
*NRF2↑,
*ROS↓,
*lipid-P↓,
*Cyt‑c↓,
*BAX↓, fig 2 antiinflammatory
*Bcl-2↓,
*iNOS↓,
*NO↓,
*IL6↓,
*IL10↓,
*IL17↓,
*IFN-γ↓,
*NF-kB↓,
*LC3II↓,
*Akt↓,
*Beclin-1↓,
*AMPK↓, fig 2 neuroprotective
*TNF-α↓,
*PGE2↓,
*Apoptosis↓,
*Casp3↓,
*Casp9↓,
*P53↓,
*P21↓,
*NAD↓, neuronal oxidative stress
*ATP↓,
*CHOP↓,
*GADD34↓,
*ATF4↓,
tumCV↓, fig 2 anticancer
Apoptosis↑,
TumCG↓,
TumCI↓,
TumMeta↓,
CSCs↓, glioma stem cells ↓b-catenin, ↓Notch-1, ↓STAT3
NOTCH1↓,
STAT3↓,
eff↑, emodin combined with curcumin ↓proliferation, ↑miR-34a
miR-34a↓,
*neuroP↑, Neuroprotective LPS-stimulated mouse ↓Nrf-2, NQO1, ↓TNF-α,↓↓ IL-6, ↓NO, ↓PGE2
*BDNF↓, model of chronic stress mice in vivo ↓progression of behavioral impairments in mice ↓consumption of sucrose, ↓plasmatic corticosterone, ↓mRNA, ↓BDNF,
*hepatoP↑, Hepatoprotective rats in vivo ↓ethanol-mediated liver steatosis ↓ ALT, ↓AST, ↓ TGL
*ALAT↓,
*AST↓,
TG/TAG↓,
ROS↑, However, at higher concentrations, emodin significantly increased ROS generation and reduced cell viability.
Slug↓, expression levels of Slug (a transcription factor) were also suppressed with emodin treatment.
EMT↓, results suggested that emodin suppressed the epithelial-mesenchymal transition of cancer cells through the ILK/GSK-3β/Slug signaling pathway
Glycolysis↓, In addition, emodin inhibited glycolysis via ROS-induced inactivation of the PI3K/AKT signaling pathway.
ChemoSen↑, The study by Peng et al. [130] also showed chemosensitizing effects of emodin to cisplatin in A549 (2–20 µM, for 48 h) and H460 (0.5–10 µM) non-small cell lung cancer cells.
P-gp↓, The sensitization mechanism was mediated by the inhibition of P-glycoprotein (Pgp), a drug-resistant protein related to the efflux pump mechanism.
Ki-67↓, The significant reduction of Ki-67 and proliferating cell nuclear antigen (PCNA) protein levels supported the antiproliferative effect of emodin in animal models.
PCNA↓,
ER Stress↑, findings suggested that emodin exerts its apoptotic effects in a process mediated by ER stress and the activation of the TRIB3/NF-κB pathway in lung cancer cells.
TRIB3↑,
NF-kB↑,
TumMeta↑, Emodin (40 mg/kg for 7 days) significantly decreased the metastatic recurrence of breast cancer after surgery in the lungs by reducing the formation of epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC).
*Imm↓, emodin may be developed as an immunosuppressive agent in case of immune activation, autoimmune disorders even in organ transplantation
*toxicity↝, An excess of emodin due to its laxative effects causes intestinal pain and severe diarrhea with subsequent electrolyte imbalance and dehydration [157]. Therefore, treatment should begin when symptoms appear, with special attention to electrolyte leve


Showing Research Papers: 1 to 50 of 103
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 103

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

ARG↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   Ferroptosis↑, 1,   GSH↓, 2,   GSH↑, 1,   HO-1↑, 1,   lipid-P↑, 1,   MDA↓, 2,   MFN2↑, 1,   NRF2↓, 1,   NRF2↑, 2,   ROS↓, 1,   ROS↑, 9,   ROS⇅, 1,   mt-ROS↑, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   CDC25↓, 1,   MMP↓, 1,   MPT↑, 1,   SDH↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↓, 1,   ATG7↑, 1,   cMyc↓, 2,   ECAR↓, 1,   FASN↓, 2,   GAPDH↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   LDHA↓, 1,   MCT4↓, 1,   PFK1↓, 1,   PKM2↓, 1,   PPARγ↑, 1,   SIRT1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 4,   p‑Akt↓, 2,   Apoptosis↑, 11,   BAX↑, 4,   Bax:Bcl2↑, 1,   Bcl-2↓, 5,   Casp↑, 1,   Casp12↑, 1,   Casp3↑, 5,   cl‑Casp3⇅, 1,   Casp8↑, 3,   Casp9↑, 3,   p‑Chk2↑, 1,   Cyt‑c↑, 4,   Diablo↑, 1,   DR5↑, 1,   Fas↑, 1,   Ferroptosis↑, 1,   ICAD↓, 1,   iNOS↓, 1,   JNK↓, 1,   MAPK↝, 1,   MCT1↓, 1,   oncosis↑, 1,   p27↑, 1,   p38↓, 1,   p38↑, 2,   survivin↓, 3,  

Kinase & Signal Transduction(tgid=6) ⓘ

miR-25-5p↓, 1,   SOX9↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,   other↝, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↑, 1,   ER Stress↑, 3,   GRP78/BiP↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   BNIP3↑, 1,   TumAuto↑, 3,  

DNA Damage & Repair(tgid=10) ⓘ

p‑ATM↑, 1,   p‑ATR↑, 1,   CHK1↓, 1,   p‑CHK1↑, 1,   DNAdam↑, 4,   HR↓, 1,   p16↑, 1,   P53↑, 6,   PARP↑, 1,   cl‑PARP↑, 2,   PCNA↓, 1,   RAD51↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

p‑CDK1↓, 1,   CDK4↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   cycE/CCNE↑, 1,   cycE1↓, 1,   P21↑, 2,   p‑RB1↓, 1,   TumCCA↑, 8,  

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

cMET↓, 1,   CSCs↓, 2,   Diff↑, 1,   EMT↓, 2,   ERK↓, 1,   p‑ERK↓, 2,   FOXM1↓, 1,   Gli1↓, 1,   GSK‐3β↓, 1,   HH↓, 1,   miR-34a↓, 1,   mTOR↓, 2,   mTOR↝, 1,   p‑mTOR↓, 1,   NOTCH1↓, 1,   PI3K↓, 1,   Smo↓, 1,   p‑Src↓, 1,   STAT3↓, 7,   TOP2↓, 1,   TumCG↓, 4,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   ARG1/2↑, 1,   cal2↓, 1,   CDK4/6↓, 1,   p‑FAK↓, 2,   ITGB1↑, 1,   Ki-67↓, 2,   MMP2↓, 4,   MMP9↓, 6,   NCAM↑, 1,   Slug↓, 1,   Smad1↓, 1,   TGF-β↓, 2,   TIMP2↑, 1,   TRIB3↑, 1,   TumCI↓, 4,   TumCMig↓, 2,   TumCP↓, 5,   TumMeta↓, 3,   TumMeta↑, 1,   Twist↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 4,   EGFR↓, 3,   Hif1a↓, 5,   KDR/FLK-1↓, 1,   NO↓, 7,   VEGF↓, 9,   VEGFR2↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GLUT1↓, 1,   P-gp↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 5,   CRP↓, 1,   HCAR1↓, 1,   IFN-γ↓, 1,   IL1↓, 1,   IL1β↓, 3,   IL6↓, 5,   IL8↓, 1,   Imm↑, 1,   Inflam↓, 1,   MIP2↓, 1,   NF-kB↓, 7,   NF-kB↑, 1,   PGE2↓, 1,   TNF-α↓, 3,  

Cellular Microenvironment(tgid=17) ⓘ

pH↑, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

ADAM10?, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   ChemoSen↑, 5,   Dose↝, 1,   eff↑, 6,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   CRP↓, 1,   E6↓, 1,   E7↓, 1,   EGFR↓, 3,   FOXM1↓, 1,   GutMicro↑, 1,   IL6↓, 5,   Ki-67↓, 2,   TG/TAG↓, 1,   TRIB3↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↓, 1,   AntiCan↑, 4,   chemoP↑, 1,   chemoPv↑, 1,   cognitive?, 1,   hepatoP↑, 1,   neuroP↑, 1,   Risk↓, 1,   toxicity↓, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 195

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 2,   TRPA1↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 2,   antiOx↑, 16,   Catalase↑, 11,   Catalase↝, 1,   Ferroptosis↓, 1,   GPx↑, 9,   GSH↑, 11,   GSR↓, 1,   GSR↑, 1,   GSTs↑, 2,   H2O2↓, 2,   HDL↑, 1,   HO-1↑, 6,   Keap1↓, 1,   lipid-P↓, 8,   MDA↓, 16,   MPO↓, 2,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 10,   RNS↓, 1,   ROS↓, 26,   SOD↑, 20,   SOD↝, 1,   TAC↑, 2,   TBARS↓, 2,   Trx1↑, 1,   VitC↑, 3,   VitE↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 1,   ATP↓, 1,   ATP↑, 1,   MEK↓, 1,   MMP↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

adiP↓, 1,   adiP↑, 1,   ALAT↓, 6,   AMPK↓, 1,   p‑AMPK↑, 1,   cAMP↑, 2,   H2S↑, 1,   LDH↓, 5,   LDL↓, 3,   NAD↓, 1,   NADPH↑, 1,   PPARα↑, 1,   PPARγ↓, 1,   SIRT1↑, 2,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Akt↑, 3,   Apoptosis↓, 8,   BAX↓, 3,   Bcl-2↓, 1,   Bcl-2↑, 1,   Casp3↓, 3,   Casp6↓, 1,   Casp9↓, 3,   Cyt‑c↓, 2,   Fas↓, 1,   Ferroptosis↓, 1,   GADD34↓, 1,   iNOS↓, 14,   iNOS↑, 1,   JNK↓, 3,   p‑JNK↓, 1,   MAPK↓, 3,   MAPK↑, 1,   p38↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

TRPV3↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1,   other↑, 2,   other↝, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↓, 2,   GRP78/BiP↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,   LC3II↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,   P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

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

ERK↑, 2,   GSK‐3β↓, 3,   HDAC↓, 1,   mTOR↓, 1,   PI3K↓, 1,   PI3K↑, 2,   STAT↓, 1,   p‑STAT1↓, 1,   p‑STAT3↓, 1,  

Migration(tgid=13) ⓘ

5LO↓, 2,   i-Ca+2↓, 1,   CLDN1↑, 1,   E-sel↓, 1,   MMP2↓, 1,   MMP3↓, 2,   MMP9↓, 1,   MMP9↑, 1,   MMPs↑, 1,   MUC1↑, 1,   SMAD3↓, 1,   TGF-β1↓, 1,   TIMP1↑, 1,   VCAM-1↓, 1,   ZO-1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 1,   EPR↑, 1,   NO↓, 43,   NO↑, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 5,   CLDN3↑, 1,   IBI↑, 1,   OCLN↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2↓, 16,   CRP↓, 1,   CXCR4↓, 1,   ICAM-1↓, 1,   IFN-γ↓, 5,   IKKα↓, 1,   IL1↓, 1,   IL10↓, 1,   IL10↑, 2,   IL12↓, 2,   IL17↓, 4,   IL1β↓, 13,   IL2↓, 2,   IL2↑, 1,   IL4↓, 1,   IL6?, 1,   IL6↓, 15,   IL8↓, 4,   Imm↓, 1,   INF-γ↓, 1,   Inflam↓, 24,   IκB↑, 1,   p‑JAK1↓, 1,   p‑JAK2↓, 1,   MCP1↓, 2,   MyD88↓, 1,   NF-kB↓, 13,   NF-kB↑, 1,   p‑NF-kB↓, 1,   PGE2↓, 12,   PGE2↑, 1,   Th1 response↓, 1,   Th2↑, 2,   TLR2↓, 1,   TLR4↓, 3,   TNF-α↓, 17,   TNF-α↑, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   AChE↓, 4,   AChE∅, 1,   BDNF↓, 1,   BDNF↑, 2,   NGF↑, 1,   tau↓, 2,   p‑tau↓, 1,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 6,   BACE↓, 1,   NLRP3↓, 3,   XO↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

GR↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 6,   AST↓, 6,   BP↓, 2,   creat↓, 1,   CRP↓, 1,   GutMicro↑, 5,   IL6?, 1,   IL6↓, 15,   LDH↓, 5,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   AntiDiabetic↓, 1,   AntiDiabetic↑, 1,   BOLD↑, 1,   cardioP↑, 8,   cognitive↑, 9,   hepatoP↓, 1,   hepatoP↑, 8,   memory↑, 10,   motorD↑, 1,   neuroP↑, 22,   Obesity↓, 1,   RenoP↑, 3,   Risk↓, 3,   toxicity↓, 3,   toxicity↝, 3,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 2,   Bacteria↓, 2,  
Total Targets: 207

Scientific Paper Hit Count for: NO, Nitric Oxide
5 Curcumin
5 Silymarin (Milk Thistle) silibinin
4 EGCG (Epigallocatechin Gallate)
4 Hydrogen Gas
4 Lycopene
4 Magnetic Fields
4 Propolis -bee glue
3 Alpha-Lipoic-Acid
3 Artemisinin
3 Melatonin
3 Quercetin
3 Sulforaphane (mainly Broccoli)
3 Thymoquinone
2 Silver-NanoParticles
2 Resveratrol
2 Ascorbyl Palmitate
2 Baicalein
2 Boron
2 Carvacrol
2 Carnosine
2 Centella asiatica / Gotu kola → asiaticoside
2 Dandelion Root
2 Fisetin
2 Piperlongumine
2 Rosmarinic acid
1 1,8-Cineole
1 Anthocyanins
1 Allicin (mainly Garlic)
1 alpha Linolenic acid
1 Andrographis
1 Apigenin (mainly Parsley)
1 Ashwagandha(Withaferin A)
1 Astaxanthin
1 Baicalin
1 Betulinic acid
1 borneol
1 Boswellia (frankincense)
1 α-Bisabolol / Chamomile oil
1 Carnosic acid
1 Chlorogenic acid
1 Chrysin
1 Crocetin
1 Carvone
1 Lecithin
1 Diclofenac
1 Emodin
1 Ferulic acid
1 Ginkgo biloba
1 Geraniol
1 HydroxyCitric Acid
1 Orlistat
1 Honokiol
1 Luteolin
1 Magnetic Field Rotating
1 Mushroom Lion’s Mane
1 Oleuropein
1 Pterostilbene
1 Sesame seeds and Oil
1 acetaminophen
1 Shikonin
1 Turmerones
1 Thymol-Thymus vulgaris
1 Wogonin
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#:563  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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