iNOS Cancer Research Results
iNOS, Inducible nitric oxide synthase: Click to Expand ⟱
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An enzyme that produces nitric oxide (NO) in response to inflammatory stimuli.
iNOS can promote tumor growth by enhancing blood flow and nutrient supply to tumors through vasodilation. It may also help cancer cells evade apoptosis (programmed cell death).
Immune Activation: In some contexts, NO produced by iNOS can enhance the immune response against tumors, promoting the activation of immune cells that can target and destroy cancer cells.
Inhibition of Tumor Growth: High levels of NO can induce cytotoxic effects on tumor cells, leading to reduced proliferation and increased apoptosis.
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Scientific Papers found: Click to Expand⟱
*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↓,
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*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 γ-glutamyl cysteine synthetase (γ-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)
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*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↓,
*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↓,
*LDH↓, ALA reduces LDH release from H2O2-induced cells
*NOX4↓, ALA downregulates the expression of Nox4
*NF-kB↓, ALA inhibits H2O2-induced activation of the NF-κB signaling pathway
*iNOS↓, ALA suppresses the upregulation of iNOS, VCAM-1 and ICAM-1 in H2O2-induced HUVECs
*VCAM-1↓,
*ICAM-1↓,
*ROS↓, ALA protected HUVECs against oxidative damage induced by H2O2, as assessed by cell viability and LDH activity.
*cardioP↑, regulating Nox4 protein expression and play a protective role in cardiovascular disease.
*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
*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
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↓,
NRF2↑,
COX2↓,
IL6↓,
IL8↓,
IL1↓, IL-1β
iNOS↓,
MPO↓,
TNF-α↓,
VEGF↓,
Hif1a↓,
p‑AMPK↑,
TNF-α↓,
IL1β↓,
IL6↓,
IL10↓,
COX2↓, blocks the nitric oxide-mediated cyclooxygenase-2 expression
iNOS↓,
Inflam↓,
Dose∅, apigenin contents were reported high in celery and parsley with amounts of 19 and 215 mg per 100 g, respectively
Dose∅, dried parsley contains highest concentration of apigenin (45,035 μg/g). The dried chamomile flowers contain 3,000 to 5,000 μg/g of apigenin.
*Inflam↓, Artemisinin has potent anti-inflammatory and immune activities.
*neuroP↑, Artemisinin inhibited neuroinflammation and exerted neuroprotective effects by regulating the Toll-like receptor 4 (TLR4)/Nuclear factor-kappa B (NF-κB) signaling pathway.
*TLR4↓,
*NF-kB↓,
*memory↑, reversing spatial learning and memory deficits.
*ROS↓, Artemisinin Decreased the Production of ROS and iNOS in BV2 Cells
*iNOS↓,
*COX2↓, Artemisinin treatment decreased the expression of COX2 and iNOS
*cognitive↑, Artemisinin Improved the Cognitive Impairment of AD Model Mice
*TNF-α↓,
*IL6↓,
*MCP1↓,
*NO↓,
*iNOS↓,
*IκB↑,
*TNF-α↓, Suppression of reactive gliosis, inflammatory cytokines production like TNF-α, IL-1β, IL-6, and expression of nitro-oxidative stress enzymes like iNOS, COX2, NOX2 etc were observed in ASH-WEX-treated animals.
*IL1β↓,
*IL6↓,
*iNOS↓,
*COX2↓,
*NOX↓,
*cognitive↑, ameliorates associated behavioral abnormalities
*Inflam↓,
*NF-kB↓, ASH-WEX-Mediated Inhibition of NFkB Pathway
*neuroP↑, fucoxanthin and astaxanthin, natural carotenoids abundant in algae, has shown to possess neuroprotective properties through antioxidant, and anti-inflammatory characteristics in modulating the symptoms of AD.
*antiOx↑,
*Inflam↑,
*AChE↓, Fucoxanthin and astaxanthin exhibit anti-AD activities by inhibition of AChE, BuChE, BACE-1, and MAO, suppression of Aβ accumulation.
*BACE↓,
*MAOA↓,
*Aβ↓,
*memory↑, Recently, Che, Li (Che et al., 2018) reported that astaxanthin possessed memory enhancement.
*MDA↓, Astaxanthin, as an antioxidant, helps to reduce oxidative stress by lowering malondialdehyde (MDA) levels and increasing SOD activity by activation of the NrF2/HO-1 pathway
*SOD↑,
*NRF2↑,
*HO-1↑,
*NF-kB↓, astaxanthin showed NFκB inhibitory activity which caused the downregulation of BACE-1 expression, resulting in Aβ reduction
*GSK‐3β↓, astaxanthin dose-dependently attenuated the GSK-3β activity
*ChAT↑, astaxanthin could reduce neuroinflammation via reducing iNOS expression and spine loss on the hippocampal CA1 pyramidal neurons, and restoring the ChAT expression in the medial septal nucleus
*iNOS↓,
*ROS↓, astaxanthin treatment decreased the ROS production and enhanced the cell growth.
*BBB↑, Astaxanthin can attenuate neurological dysfunction because of its unique chemical structure and can cross the BBB to enter the brain tissue
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*neuroP↑, Recent studies have shown its good protective effect on neurons and brain tissues [14].
*antiOx↑, strong anti-inflammatory and antioxidant properties.
*Inflam↓,
*BioAv↝, When taken orally, baicalin is converted to baicalein via β-glucuronidase (GUS), which is produced by the intestinal flora.
*BioAv↑, Pharmacokinetics indicate that baicalein has a higher absorption rate than baicalein [19], but once it is absorbed, baicalein is quickly degraded in the bloodstream, yielding baicalein
*Half-Life↝, The distribution half-life and elimination half-life of baicalin in the CSF of normal rats are 0.8868 and 26.0968 min, respectively.
*TLR4↓, Inhibition of the TLR4/MyD88/NF-κB signal
*NF-kB↓,
*iNOS↓, decreasing the synthesis of iNOS, COX2, and TNF-α
*COX2↓,
*TNF-α↓,
*12LOX↓, downregulation of 12/15-LOX after cerebral ischemia
*NLRP3↓, Inhibition of the expression of NLRP3, HT-22 cells
*ROS↓, Decrease in the ROS levels in the ICH, thus inhibiting high NLRP3
*IL1β↓, Reduced the amounts of IL-1β and IL-6 and inhibited the activation of the NLRP3 inflammasome
*IL6↓,
*GSK‐3β↓, Inhibiting the activation of the GSK3β/NF-κB/NLRP3 signaling pathway
*NRF2↑, Fang et al. reported that the activation of the Akt pathway resulted in increased Nrf2 nuclear translocation and immunoreactivity in a group treated with baicalin
*BBB↑, baicalein effectively crosses the blood‒brain barrier (BBB) and stimulates the Nrf2/HO-1 pathway via specialized brain-targeted exosomes
*SOD↑, increased serum levels of SOD and GSH-Px.
*GPx↑,
*MDA↓, baicalin inhibited the ROS production and reduced MDA levels in brain tissues from a rat model of cerebral I/R injury induced by middle cerebral artery occlusion (MCAO).
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*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
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ROS⇅, Like other flavonoids, baicalein can be either anti-oxidant or pro-oxidant, depending on its metabolism and concentration.
ROS↑, It is reported that baicalein generated ROS, subsequently caused endoplasmic reticulum (ER) stress, activated Ca2+-dependent mitochondrial death pathway, finally triggered apoptosis
ER Stress↑,
Ca+2↑,
Apoptosis↑,
eff↑, Due to this, ROS production is a mechanism shared by all non-surgical therapeutic approaches for cancer, including chemotherapy, radiotherapy and photodynamic therapy
DR5↑, baicalein-induced ROS generation up-regulated DR5 expression and then activated the extrinsic apoptotic pathway in human prostate cancer cells
12LOX↓, Baicalein is known as a 12-LOX inhibitor.
Cyt‑c↑, It markedly induced the release of Cytochrome c from mitochondria into the cytosol and activated Caspase-9, Caspase-7, and Caspase-3, concomitant with cleavage of the Caspase-3 substrate poly(ADP-ribose) polymerase
Casp7↑,
Casp9↑,
Casp3↑,
cl‑PARP↑,
TumCCA↑, Baicalein induces G1/S arrest due to increased Cyclin E expression, a major factor in the regulation of the G1/S checkpoint of the cell cycle, accompanied by reduced levels of Cdk 4 and Cyclin D1 in human lung squamous carcinoma (CH27) cells
cycE/CCNE↑,
CDK4↓,
cycD1/CCND1↓,
VEGF↓, In ovarian cancer cells, baicalein effectively lowered the protein level of VEGF, c-Myc, HIF-α, and NFκB
cMyc↓,
Hif1a↓,
NF-kB↓,
BioEnh↑, curcumin and high-dose (−)-epicatechin were demonstrated to subsequently increase the absorption of baicalein
BioEnh↑, Baicalein can increase the oral bioavailability of tamoxifen by inhibiting cytochrome P450 (CYP) 3A4-mediated metabolism of tamoxifen in the small intestine and/or liver,
P450↓,
*Hif1a↓, In BV2 microglia, baicalein suppressed expression of hypoxia-induced HIF-1α and hypoxia responsive genes, including inducible nitric oxide synthase (iNOS), COX-2, and VEGF, by inhibiting ROS and PI3K/Akt pathway (Hwang et al. 2008).
*iNOS↓,
*COX2↓,
*VEGF↓,
*ROS↓,
*PI3K↓,
*Akt↓,
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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↓,
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*BioAv↓, Biochanin A (BCA) is an isoflavone mainly found in red clover with poor solubility and oral absorption
*Inflam↓, various effects, including anti-inflammatory, estrogen-like, and glucose and lipid metabolism modulatory activity, as well as cancer preventive, neuroprotective, and drug interaction effects.
AntiCan↑,
*neuroP↑, many studies have focused on the effect of BCA on neurodegenerative diseases, especially PD and AD
chemoPv↑, BCA Has Chemopreventive Activity Against Various Cancers
Dose↝, BCA is metabolized in the gut to GEN or formononetin, which is converted to daidzein and then to equol (Knight and Eden, 1996).
*SOD↑, BCA also has a gastroprotective effect through the enhancement of cellular metabolic cycles, as evidenced by increases in superoxide dismutase (SOD) and nitric oxide (NO) activity, decreases in the malondialdehyde (MDA) and Bax levels, and increases
*MDA↓,
*BAX↓,
*HSP70/HSPA5↑, and increases in Hsp70 expression
*AntiDiabetic↑, BCA is well known for its antidiabetic and hypolipidemic effects.
*Insulin↑, BCA increases the circulating insulin levels and improves insulin sensitivity, leading to body weight control, an increase in liver glycogen, and a decrease in plasma glucose
*TNF-α↓, BCA inhibits the production of inflammatory mediators, such as TNF-α, interleukin-1β (IL-1β), IL-6, iNOS, COX-2, MMP-9, and NO, in various inflammatory responses
*IL1β↓,
*IL6↓,
*iNOS↓,
*COX2↓,
*MMP9↓,
*ROS↓, BCA scavenges ROS and increases SOD activity
*PGE2↓, BCA significantly reduces the synthesis of prostaglandin E2 and/or thromboxane B2 by inhibiting COX-2 expression
*BACE↓, BCA effectively inhibits the activity of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1)
*BioAv↑, Various attempts have been made to improve the solubility and bioavailability of BCA, including the use of liposomes
P-gp⇅, Interestingly, BCA has been found to stimulate P-gp in some studies (An and Morris, 2010). Therefore, the effect of BCA on P-gp may be substrate dependent.
*CB2 / CNR2↑, selective cannabinoid receptor 2 (CB2) agonist
*Bacteria↓, numerous pharmacological activities such as antibacterial (e.g., Helicobacter pylori), antioxidant, anti-inflammatory, analgesic (e.g., neuropathic pain), anti-neurodegenerative and anticancer properties.
*antiOx↑,
*Inflam↓,
*NP/CIPN↓,
*neuroP↑,
AntiCan↑,
*ROS↓, β-caryophyllene in reducing oxidative stress and mitochondrial dysfunction, and its possible links with neuroprotection.
*mtDam↓,
*GSH↑, β-caryophyllene (50 mg/kg/day, i.p. for 4 weeks) ↑ GSH, SOD and CAT. Inhibit lipid peroxidation. ↓ IL-1β, IL-6, and TNF-α levels. ↓ COX-2 and iNOS expression.
*SOD↑,
*Catalase↑,
*lipid-P↓,
*IL1β↓,
*IL6↓,
*TNF-α↓,
*COX2↓,
*iNOS↓,
*NRF2↑, β-caryophyllene (34, 102 and 306 mg/kg/day, p.o.). ↑ Nrf2 and HO-1 expression. Restored SOD and CAT activity and expression.
*HO-1↑,
*AChE↓, Syzygium aromaticum (L.) Merr. and L.M. Perry (0.05 mL/kg and 0.1 mL/kg) ↓ AChE activity, lipid peroxidation levels
*CB2 / CNR2↑, is a selective phytocannabinoid agonist of type 2 receptors (CB2-R)
*Inflam↓, via inhibiting the main inflammatory mediators, such as inducible nitric oxide synthase (iNOS), Interleukin 1 beta (IL-1 beta), Interleukin-6 (IL-6), tumor necrosis factor-alfa (TNF-alpha)
*iNOS↓,
*IL1β↓,
*IL6↓,
*TNF-α↓,
*NF-kB↓, NF-kappa B), cyclooxygenase 1 (COX-1), cyclooxygenase 2 (COX-2). P
*COX1↓,
*COX2↓,
*PPARα↑, activation of PPAR-alpha and PPAR-gamma receptors.
*PPARγ↑,
*BioEnh↑, Nevertheless, it inhibits various cytochrome P450 isoforms (above all, CYP3A4), which metabolise xenobiotics, leading to adverse effects, due to drug levels over therapeutic window.
*neuroP↑, β-caryophyllene and xanthohumol have demonstrated significant neuroprotective potential in preclinical models.
*BioAv↝, advanced drug-delivery systems, including polymer- and lipid-based nano- and microscale carriers. Such advancements not only enhance the bioavailability and therapeutic potential of these phytochemicals
*CB2 / CNR2↑, selective agonist of cannabinoid type 2 receptors (CB2-R)
*Inflam↓, BCP demonstrates anti-inflammatory properties by suppressing key inflammatory mediators, including inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB),
*iNOS↓,
*IL1β↓,
*IL6↓,
*TNF-α↓,
*NF-kB↓,
*COX1↓, and cyclooxygenases COX-1 and COX-2.
*COX2↓,
*PPARα↑, actions are partly mediated through activation of peroxisome proliferator-activated receptors, particularly PPAR-α and PPAR-γ.
*PPARγ↑,
*ROS↓, decreased the generation of reactive oxygen species (ROS)
*tau↓, XAN has been shown to directly inhibit the fibrillization tau protein and disaggregate existing fibrils, effectively reducing tau-induced apoptosis in cellular models of AD
*NRF2↑, XAN has been consistently shown to activate the Nrf2/HO-1 pathway, enhancing antioxidant defenses and reducing reactive oxygen species (ROS) levels
*HO-1↑,
*AChE↓, XAN: its ability to inhibit cholinesterases (AChE and BChE) supports its potential for symptomatic treatment of AD,
*BChE↓,
*BioAv↓, XAN’s clinical translation is hindered by poor oral bioavailability and limited BBB penetration.
TumCG↓, showed lower cell growth, underwent apoptosis and lost the ability to metastasis through the suppression of NF-ҡ B via PI3K/AKT signalling pathway.
Apoptosis↑,
TumMeta↓,
NF-kB↓,
PI3K↓,
Akt↓,
ROS↑, BCP (20, 40 and 60 mg/ml) shows significantly increased levels of ROS generation
MMP↓, Loss of MMP was visualised by Rh-123 staining
DNAdam↑, BCP-induced oxidative DNA damage
BAX↑, KB cells treated with BCP showed significant (p < .05) increased level of Bax and casapse-3, 9 and diminished expressions of mutant-p53, Bcl-2, PCNA and cyclin-D1
Casp3↑,
Casp9↑,
Bcl-2↓,
PCNA↓,
cycD1/CCND1↓,
TNF-α↓, NF-jB, TNF-a, COX-2, iNOS, IL-6 and VEGF, while treatment with different concentration of BCP (20, 40
and 60 mg/ml) significantly (p < .05) down-regulated the expression of the above mentioned protein markers
COX2↓,
iNOS↓,
IL6↓,
VEGF↓,
*Inflam↓, anticancer, anti-edema, anti-inflammatory, anti-microbial, anti-coagulant, anti-osteoarthritis, anti-trauma pain, anti-diarrhea, wound repair.
*Bacteria↓,
*Pain↓,
*Diar↓,
*Wound Healing↑,
ERK↓, Figure 1
JNK↓,
XIAP↓,
HSP27↓,
β-catenin/ZEB1↓,
HO-1↓,
lipid-P↓,
ACSL4↑,
ROS↑,
SOD↑,
Catalase↓,
GSH↓,
MDA↓,
Casp3↓,
Casp9↑,
DNAdam↑,
Apoptosis↑,
NF-kB↓,
P53↑,
MAPK↓,
APAF1↑,
Cyt‑c↓,
CD44↓,
Imm↑, Bromelain was also studied in the innate immune system, where it could enhance and sustain the process
ATG5↑,
LC3I↑,
Beclin-1↑,
IL2↓, bromelain in vitro experiments resulted in diminished amounts of IL-2, IL-6, IL-4, G-CSF, Gm-CSF, IFN-γ,
IL4↓,
IFN-γ↓,
COX2↓, proprietary bromelain extract could decrease IL-8, COX-2, iNOS, and TNF-α without affecting cell viability.
iNOS↓,
ChemoSen↑, Bromelain may increase the cytotoxicity of cisplatin in the treatment of breast cancer as reported in 2 studies with MDA-MB-231 and 4T1 Breast Tumor cell lines
RadioS↑, The size and weight of tumors in gamma-irradiated EST-bearing mice treated with bromelain decreased significantly with a significant amelioration in the histopathological examination
Dose↝, oral bromelain administration in breast cancer patients (daily up to a dose of 7800 mg)
other↓, The role of bromelain (in combination with papain, sodium selenite and Lens culinaris lectin) has been also tested as a complementary medicine on more than 600 breast cancer patients to reduce the side effects caused by the administration of the adju
*TNF-α↓, supplemental boron displayed decreased levels of TNF-alpha (a), IL-1ß, MIP-1a, and iNOS expression. Each of these factors is under NF-kappa (k) B control.
*IL1β↓,
*MIP‑1α↓,
*iNOS↓,
*NF-kB↓,
*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↓,
*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)
Risk↓, Rats treated with BJe showed a significant dose-related reduction in the colon preneoplastic lesions mucin-depleted foci (MDF). strategy to prevent CRC in high-risk patients.
TumMeta↓, Colon and small intestinal tumours were also significantly reduced in rats supplemented with 70 mg/kg of BJe.
Apoptosis↑, Moreover, in colon tumours from rats fed with 70 mg/kg BJe, apoptosis was significantly higher than in controls.
COX2↓, significant down-regulation of inflammation-related genes (COX-2, iNOS, IL-1β, IL-6 and IL-10 and Arginase 1).
iNOS↓,
IL1β↓,
IL6↓,
IL10↓,
P53↑, Up-regulation of p53 and down-regulation of survivin and p21 genes was also observed.
P21↓,
survivin↓,
chemoPv↑, These data indicate a strong chemopreventive activity of BJe that, at least in part, is due to its pro-apoptotic and anti-inflammatory actions.
*Inflam↓,
*antiOx↑, (-)-α-bisabolol is a monocyclic sesquiterpene alcohol found in various plants and mainly in Matricaria chamomilla, which exerts antioxidant, anti-inflammatory, and anti-apoptotic activities.
Inflam↓, (-)-α-bisabolol provides neuroprotective action probably due to its anti-inflammatory activity, although other mechanisms cannot be discarded.
*Dose↝, Animals were treated with (-)-α-bisabolol (50, 100 and 200 mg/kg/day, orally) or vehicle (3% tween 80) one day before and 1 h after pMCAO and the treatment continued once daily for the following five days.
*neuroP↑, treatment with (-)-α-bisabolol (100 and 200 mg/kg) significantly reduced the infarcted area and neurological deficits caused by pMCAO
*motorD↑, (-)-α-bisabolol also increased the locomotor activity which was reduced by cerebral ischemia and improved pMCAO-induced working, spatial, object recognition, and aversive memories deficits.
*memory↑,
*MPO↓, (-)-α-bisabolol (200 mg/kg) significantly prevented the increase of myeloperoxidase (MPO) activity, TNF-α immunoreactivity in the temporal cortex, and the increase of iNOS both in the temporal cortex and in the striatum.
*TNF-α↓,
*iNOS↓,
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AntiCan↑, Numerous experimental studies demonstrated pharmacological properties of α-Bisabolol including anticancer, antinociceptive, neuroprotective, cardioprotective, and antimicrobial.
*neuroP↑,
*cardioP↑,
*AntiBio↑,
*BioAv↑, Given the polypharmacological effects and pleiotropic properties, along with favorable pharmacokinetics, and dietary availability and safety, α-Bisabolol can be used as a dietary agent, nutraceutical or phytopharmaceutical agent or as an adjuvant wit
*toxicity↓,
*BioAv↑, integrated in many cosmetic formulations due to its skin soothing effects, well documented dermal absorption
*motorD↑, improvement in locomotor activity, a reduction in the expression of thiol and a reinstate of the activity of mitochondrial complex-I.
*SOD↑, α-Bisabolol also increased the mRNA level of antioxidants proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product.
*Catalase↑,
*Keap1↑,
*MDA↓, α-Bisabolol attenuated oxidative insult by reducing malondialdehyde (MDA), restoring depleted glutathione (GSH) and improving SOD and CAT activity.
*GSH↑,
*IL1β↓, attenuated neuroinflammation by reducing glial cells activation and subsequent release of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and mediators (iNOS and COX-2).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2↓,
*lipid-P↓, α-Bisabolol restored mitochondrial function by preventing mitochondrial lipid peroxidation, cytochrome-C release and most importantly preserving Complex-I activity
*Cyt‑c↓,
*ROS↓, The study concluded that α-Bisabolol safeguarded against the induced upsurge of ROS and nitrite.
*MMP↑, α-Bisabolol treatment also restored mitochondrial membrane potential (MMP) validating its antioxidant effect.
*antiOx↑,
*AChE↓, showed a significant reduction in AChE activity and an ability to avert Ach depletion.
*Apoptosis↓, α-Bisabolol protected cells from Aβ triggered apoptosis by reducing Bax and Caspase-3 and increasing Bcl-2 activity.
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BACE↓, α-Bisabolol inhibitory activity on BACE1 and found a decrease in BACE1 activity following α-Bisabolol treatment
*BChE↓, AChE, BuChE, β-secretase actions were decreased significantly in cells pretreated with α-Bisabolol
*eff↑, The compound clearly illustrated a potent anti-AchE activity of 95.869% similar to the activity of donepezil, a standard drug. I
*Aβ↓, The compound also disaggregated Aβ25–35 peptide and protected against its induced toxicity by increasing neuro2a cells viability [
*ATP↑, figure 2
RadioS↑, α-Bisabolol and Anticancer Effects, figure 3
Cyt‑c↑,
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↑,
PARP↑,
BAX↑,
BID↑,
NF-kB↑,
Fas↑,
EGFR↑,
TIMP2↑,
XIAP↓,
COX2↓,
Bak↓,
Bcl-2↓,
P53↑, The expression of p53 (a transcription factors whose products might lead to apoptosis), NF-κB and Fas was increased following α-Bisabolol treatment, indicating their function in mediating α-Bisabolol-induced apoptosis in the cancer cell line.
HER2/EBBR2↓,
FGF↓,
CEA↓,
Akt↓,
TumCCA↑, α-Bisabolol suppresses the cellular proliferation at G2/M cell cycle phase.
*Imm↑, reported that α-Bisabolol boosted the immunity response by T-cell subsets (CD4 and CD8) supplementation in treated mice.
*CD4+↑,
*CD8+↑,
*BBB↑, ↑ BBB penetration
*Pain↓, α-Bisabolol based mouthwash to that of chlorhexidine in reducing pain during brushing
*cardioP↑, α-Bisabolol and Cardioprotection, figure 5
*TBARS↓, rats co-treated with α-Bisabolol showed reduced LOOH and TBARS and increased SOD, CAT and GSH.
*SOD↑,
*Catalase↑,
*GSH↑,
*AntiBio↑, α-Bisabolol demonstrated an antibacterial effect against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa as well as a synergism against S. aureus, when combined with the antibiotic norfloxacin and against E. coli when combined with
*AntiFungal↑, ↓ fungal growth
*GastroP↑, α-Bisabolol and Gastroprotection. oral administration of α-Bisabolol was realized to attenuate gastric damage and to provide cytoprotection in stomach.
*RenoP↑, The nephroprotective effects of α-Bisabolol and the underlying mechanisms are summarized in Table 10.
*creat↓, ↓ creatinine, urea, uric acid
*uricA↓,
*Inflam↓, Anti-Inflammatory Effects of α-Bisabolol
*iNOS↓, ↓ iNOS, COX-2, TNF-α, p65 PGE2, nitrite, IL-6, ↓ MMP13
*COX2↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,
*ROS↓, Various therapeutic and biological properties of α-bisabolol in preventing oxidative stress, inflammatory disorders, infections, neurodegenerative diseases, cancers, and metabolic disorders have been reported.
*Inflam↓,
*Inf↓,
*neuroP↑,
*RNS↓, The antioxidant mechanism of α-bisabolol is mainly associated with the reduction of ROS/RNS, MDA, and GSH depletion, MPO activity, and augmentation of SOD and CAT.
*MDA↓,
*GSH↑,
*MPO↓,
*SOD↑,
*Catalase↑,
*Bcl-2↑, upregulating the expression of bcl-2 and suppression of bax, P53, APAF-1, caspase-3, and caspase-9 activity indicates the anti-apoptotic effects of α- bisabolol.
*BAX↓,
*P53↓,
*APAF1↓,
*Casp3↓,
*Casp9↓,
*TNF-α↓, It possesses anti-inflammatory effects via reduction of TNF-α, IL-1β, IL-6, iNOS, and COX-2 and suppresses the activation of ERK1/2, JNK, NF-κB, and p38.
*IL1β↓,
*IL6↓,
*iNOS↓,
*COX2↓,
*ERK↓,
*JNK↓,
*NF-kB↓,
*p38↓,
*cognitive↑, improves cognitive function via downregulation of bax, cleaved caspases-3 and 9 levels, β-secretase, cholinesterase activities, and upregulation of bcl-2 levels.
*BChE↓,
Dose∅, Black chokeberries seem to be the most potent source of caffeic acid (645 mg/100 g of dry weight)
ROS⇅, Therefore, we will mention the antioxidant (and prooxidant) effects of caffeic acid only briefly
NF-kB↓, In HepG2 cells, caffeic acid (100 µM) inhibited the activity of NF-κB/IL-6/STAT3 signaling, which decreased the expression of VEGF
STAT3↓,
VEGF↓,
MMP9↓, inhibited another downstream product of NF-κB: matrix metalloproteinase 9 (MM-9), which promotes tumor invasiveness and metastases
HSP70/HSPA5↑, caffeic acid (20 μM) also decreased the expression of mortalin(mitochondrial 70 kDa heat shock protein),
AST↝, normalized levels of alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bile acid, total cholesterol, HDL and LD
ALAT↝,
ALP↝,
Hif1a↓,
IL6↓,
IGF-1R↓,
P21↑,
iNOS↓,
ERK↓,
Snail↓,
BID↑,
BAX↑,
Casp3↑,
Casp7↑,
Casp9↑,
cycD1/CCND1↓,
Vim↓,
β-catenin/ZEB1↓,
COX2↓,
ROS↑, the chelating ability of caffeic acid is also responsible for its occasional pro-oxidant ability. After chelating Cu2+, the Cu2+ can be reduced to Cu+. combination of caffeic acid and endogenous copper ions can result in oxidative damage
*antiOx↑, Carnosic acid (CA) has been reported to possess antioxidative properties
*Weight↑, CA significantly prevented the loss of body weight and shortening of colon length in acute colitis induced by dextran sodium sulfate (DSS).
*p65↓, CA decreased the activation of p65 and c-Jun signalling.
*cJun↓,
*NLRP3↓, CA inhibited DSS-induced NLRP3 inflammasome activation by reducing caspase 1 activity.
*Casp1↓,
*NRF2↑, CA increased the level of Nrf2 and prevented the degradation of Nrf2 via ubiquitination by blocking the interaction between Cullin3 and Keap1,
*GSH↑, Finally, GSH levels and SOD activity were increased after CA treatment, while MDA and iNOS levels were significantly reduced.
*SOD↑,
*MDA↓,
*iNOS↓,
other↝, Moreover, many compounds from natural products, such as ellagic acid, gallic acid and quercetin, have been shown to prevent IBD through their antioxidative properties
iNOS↓,
IL6↓,
SOX9↑,
NF-kB↓,
MAPK↓,
*NRF2↑, CA treatment alleviated depressive behavior, induced the expression of Nrf2, HO-1, thioredoxin-1, and brain-derived neurotrophic factor, and enhanced serotonin levels.
*HO-1↑,
*Trx1↑,
*BDNF↑,
*5HT↑,
*ROS↓, CA also suppressed oxidative stress, reduced TNF-α, IL-1β, and iNOS mRNA expression, and ameliorated OVX-induced histopathological changes.
*TNF-α↓,
*IL1β↓,
*iNOS↓,
HO-1↑, capsaicin induced the expression of HO-1 in human hepatoma HepG2 cells through the generation of ROS and subsequent activation of a redox-sensitive transcription factor nuclear factor erythroid related factor-2 (Nrf2)
ROS↑,
NRF2↑,
*lipid-P↓, capsaicin inhibits lipid peroxidation by increasing the activity of a battery of antioxidant enzymes
*SOD↑, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR)
*Catalase↑,
*GPx↑,
*GSR↑,
*PGE2↓, inhibitory effects of capsaicin on the production of prostaglandin E2 (PGE2) in macrophages incubated with LPS or TPA (
*COX2↓, the inhibition of COX-2 and iNOS expression by capsaicin in these cells is mediated in a VR1/TRPV1-independent manner
*iNOS↓,
TumCP↓, anticancer effects of capsaicin are partly mediated through the inhibition of cancer cell proliferation.
TumCCA↑, Capsaicin inhibited the growth of human esophageal epidermoid carcinoma (CE 81T/VGH) cells by arresting the cell cycle at the G1 phase through the downregulation of cyclin E, cyclin dependent kinase (Cdk)-4 and -6,
cycE/CCNE↓,
CDK4↓,
MMP↓, Similarly, the inhibition of Cdk-2,-4 and-6, the generation of ROS, and the loss of mitochondrial membrane potential were associated with reduced proliferation of human bladder cancer cells upon capsaicin treatment
P53↑, capsaicin is mediated through the induction of p53 nd its target gene products such as, p21, and Bax.
P21↑,
BAX↑,
SIRT1↑, The same study also demonstrated that capsaicin induced autophagy in human fetal lung cells by inducing SIRT1
angioG↓, Capsaicin inhibited angiogenesis in the chick chorioallantoic membrane
P-gp↓, Capsaicin inhibited the P-gp activity in human intestinal carcinoma (Caco2) cells in a concentration- and time-dependent manner (
ChemoSen↑, Capsaicin exhibited synergistic growth inhibitory effects with 5-fluorouracil (5FU) in cholangiocarcinoma cells in culture as well as xenograft tumor growth in nude mice
chemoPv↑, Capsaicin has shown significant prospects as an effective chemopreventive agent
Ca+2↑, Capsaicin was shown to cause upstream activation of Ca2+
antiOx↑, Another plausible mechanism implicated in the chemopreventive action of capsaicin is its anti-oxidative effects.
*ROS↓, capsaicin inhibits ROS release and the subsequent mitochondrial membrane potential collapse, cytochrome c expression, chromosome condensation, and caspase-3 activation induced by oxidized low-density lipoprotein in normal human HUVEC cells
*MMP∅,
*Cyt‑c∅,
*Casp3∅,
*eff↑, dietary curcumin and capsaicin concurrent administration in high-fat diet-fed rats were shown to mitigate the testicular and hepatic antioxidant status by increasing GSH levels, glutathione transferase activity, and Cu-ZnSOD expression
*Inflam↓, Anti-inflammation is another mechanism implicated in the chemopreventive action of capsaicin.
*NF-kB↓, inhibition of NF-kB by capsaicin
*COX2↓, compound elicits COX-2 enzyme activity inhibition and downregulation of iNOS
iNOS↓,
TRPV1↑, major pro-apoptotic mechanisms of capsaicin is via the vanilloid receptors, primarily TRPV1
i-Ca+2?, causing a concomitant influx of Ca2+: severe condition of mitochondria calcium overload. at high concentration (> 10 µM), capsaicin induces a slow but persistent increase in intracellular Ca2+
MMP↓, depolarization of mitochondria membrane potential
Cyt‑c↑, release of cytochrome C
Bax:Bcl2↑, activation of Bax and p53 through C-jun N-terminal kinase (JNK) activation
P53↑,
JNK↑,
PI3K↓, blocking the Pi3/Akt/mTOR signalling pathway, capsaicin increases levels of autophagic markers (LC3-II and Atg5)
Akt↓,
mTOR↓,
LC3II↑,
ATG5↑,
p62↑, enhances p62 and Fap-1 degradation and increases caspase-3 activity to induce apoptosis in human nasopharyngeal carcinoma cells
Fap1↓,
Casp3↑,
Apoptosis↑,
ROS↑, generation of ROS in human hepatoma (HepG2 cells)
MMP9↓, inhibition of MMP9 by capsaicin occurs via the suppression of AMPK-NF-κB, EGFR-mediated FAK/Akt, PKC/Raf/ERK, p38 MAPK, and AP-1 signaling pathway
eff↑, capsaicin 8% patch could promote the regeneration and restoration of skin nerve fibres in chemotherapy-induced peripheral neuropathy in addition to pain relief
eff↓, capsaicin has shown several unpleasant side effects, including stomach cramps, skin and gastric irritation, and burning sensation
eff↑, liposomes and micro-emulsion-based drugs have been known to significantly improve oral bioavailability and reduce the irritation of drugs
selectivity↑, In addition, these delivery systems can be surfaced-modified to perform site-directed/cell-specific drug delivery, thereby ensuring increased cell death of cancer cells while sparing non-selective normal cells
eff↑, Furthermore, owing to its antioxidant potential, capsaicin has been applied as a bioreduction and capping agent to synthesize biocompatible silver nanoparticles
ChemoSen↑, capsaicin has been combined with other anticancer therapies for more pronounced anticancer effects
| - |
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?,
TNF-α↓, Celastrol suppresses the release of the proinflammatory cytokines TNF-α, IL-1β, and IL-6; inhibits the PKM2-dependent Warburg effec
IL1β↓,
IL6↓,
Warburg↓,
PKM2↓,
NRF2↑, Additionally, celastrol activates the NRF2/HO-1 pathway, inhibits the activation of NF-κB, and reduces the expression of TNF-α, IL-6, IL-1β, and iNOS, further suppressing M1 polarization
HO-1↑,
NF-kB↓,
iNOS↓,
M1↓, further suppressing M1 polarization
*antiOx↑, mainly shown as anti-oxidant, liver and kidney protection, anti-bacterial, anti-tumor, regulation of glucose metabolism and lipid metabolism, anti-inflammatory, protection of the nervous system,
*hepatoP↑,
*RenoP↑,
AntiTum↑,
*glucose↝,
*Inflam↓,
*neuroP↑,
*ROS↓, ↓Active oxygen (ROS) , ↓Keap1,↑Nrf2, ↑SOD, ↑CAT, ↑Glutathione Peroxidase (GSH-Px), ↑Glutathione (GSH), ↓MDA
*Keap1↓,
*NRF2↑,
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*MDA↓,
*p‑ERK↑, ↑ERK1/2 phosphorylation
*GRP78/BiP↑, ↑Glucose regulatory protein 78 (GRP78)
*CHOP↑, ↑C/EBP homologous protein (CHOP)
*GRP94↑, ↑Glucose Regulatory Protein 94 (GRP94)
*Casp3↓, ↓Caspase-9/Caspase-3
*Casp9↓,
*HGF/c-Met↑, ↑Hepatocyte Growth Factor (HGF)
*TNF-α↓, ↓Tumor Necrosis Factor-α (TNF-α)/Interferonγ (IFN-γ)
*TLR4↓, ↓TLR4
*MAPK↓, ↓MAPK signal pathway
*IL1β↓, ↓Interleukin 1β (IL-1β)/Interleukin 6 (IL-6)
*iNOS↓, ↓Inducible Nitric Oxide Synthase (iNOS)
TCA↓, ↓Tricarboxylic acid cycle (TCA) ↓Glycolysis
Glycolysis↓,
Bcl-2↓, ↓Anti-apoptotic gene Bcl-2/Bcl-XL
BAX↑, ↑Pro-apoptotic gene Bax/Bcl-XS/Bad
MAPK↑, ↑p38 mitogen-activated protein kinase (p38 MAPK)
JNK↑, ↑c-Jun N-terminal Kinase (JNK)
CSCs↓, ↓Stem cell marker genes Nanog, POU5F1, Sox2, CD44, Oct4
Nanog↓,
SOX2↓,
CD44↓,
OCT4↓,
P53↑, ↑P53
P21↑, ↑p21
*SOD1↑, ↑CuZnSOD (SOD1)/MnSOD (SOD2)
*AGEs↓, ↓Glycosylation end products (AGEs)
*GLUT2↑, ↑Glucose Transporter 2 (GLUT2)
*HDL↑, ↑High-density lipoprotein (HDL)
*Fas↓, ↓Fatty acid synthase (FAS)
*HMG-CoA↓, ↓β-hydroxy-β-methylglutamyl-CoA (HMG-CoA) reductase
*NF-kB↓, ↑NF-κB signaling pathway
*HO-1↓, ↑Nrf2/HO-1 signaling pathway
*COX2↓, ↓Cyclooxygenase-2 (COX-2)
*TLR4↓, ↓Toll-like receptor 4 (TLR4)
*BioAv↑, One route may be immediate absorption in the stomach or upper gastrointestinal tract, and the other route may be slowly absorbed throughout the small intestine.
*BioAv↝, It indicates that the bioavailability of CGA is closely related to the metabolic capacity of the organism's gut flora
TumCP↓, CGA also inhibits the proliferation, migration, and invasion of cancer cells.
TumCMig↓,
TumCI↓,
ROS↓, Cocoa has been demonstrated to counteract oxidative stress and to have a potential capacity to interact with multiple carcinogenic pathways involved in inflammation, proliferation and apoptosis of initiated and malignant cells
Inflam↓,
TumCP↓,
Apoptosis↑,
*Dose↝, highest flavanol content of all foodstuffs on a weight basis and is a significant contributor to the total dietary intake of flavonoids
*BioAv↓, comparison to other flavonoid-containing foodstuffs, cocoa and its derivative products exhibit a high concentration of larger procyanidins that are poorly absorbed through the gut barrier,
*BioAv↑, hose oligomers and polymers of flavanols that are not absorbed in the intestine could be metabolized by the microbiota into low molecular weight phenolic acids, which are more bioavailable, and might be well absorbed through the colon
GSH↑, Caco-2 10 µg/mL acrylamide-incubated cells: ↓ GSH depletion, ↓ ROS generation, ↑ γ-GCS, ↑ GST
GSTs↑,
PGE2↓, Caco-2 50 µM (gallic acid equivalents, 14.5 µg/mL) ↓ PGE2, ↑ COX-1,
COX1↑,
IL8↓, Caco-2 10 µg/mL TNF-treated cells: ↓ IL-8, ↓ COX-2, ↓ iNOS, ↓ NFκB activation
COX2↓,
iNOS↓,
NF-kB↓,
chemoP↑, This review reports the potential chemopreventive actions of cocoa and its main flavanols against colon cancer
*NF-kB↓, suppressed pro-inflammatory cytokine expression and histamine release, downregulated nuclear factor kappa B (NF-kB), cyclooxygenase 2 (COX-2), and inducible nitric oxide synthase (iNOS)
*COX2↓,
*iNOS↓,
angioG↓, upregulated apoptotic pathways [28], inhibited angiogenesis [29] and metastasis formation
TOP1↓, suppressed DNA topoisomerases [31] and histone deacetylase [32], downregulated tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β)
HDAC↓,
TNF-α↓,
IL1β↓,
cardioP↑, promoted protective signaling pathways in the heart [34], kidney [35] and brain [8], decreased cholesterol level
RenoP↑,
neuroP↑,
LDL↓,
BioAv↑, bioavailability of chrysin in the oral route of administration was appraised to be 0.003–0.02% [55], the maximum plasma concentration—12–64 nM
eff↑, Chrysin alone and potentially in combination with metformin decreased cyclin D1 and hTERT gene expression in the T47D breast cancer cell line
cycD1/CCND1↓,
hTERT/TERT↓,
MMP-10↓, Chrysin pretreatment inhibited MMP-10 and Akt signaling pathways
Akt↓,
STAT3↓, Chrysin declined hypoxic survival, inhibited activation of STAT3, and reduced VEGF expression in hypoxic cancer cells
VEGF↓,
EGFR↓, chrysin to inhibit EGFR was reported in a breast cancer stem cell model [
Snail↓, chrysin downregulated MMP-10, reduced snail, slug, and vimentin expressions increased E-cadherin expression, and inhibited Akt signaling pathway in TNBC cells, proposing that chrysin possessed a reversal activity on EMT
Slug↓,
Vim↓,
E-cadherin↑,
eff↑, Fabrication of chrysin-attached to silver and gold nanoparticles crossbred reduced graphene oxide nanocomposites led to augmentation of the generation of ROS-induced apoptosis in breast cancer
TET1↑, Chrysin induced augmentation in TET1
ROS↑, Pretreatment with chrysin induced ROS formation, and consecutively, inhibited Akt phosphorylation and mTOR.
mTOR↓,
PPARα↓, Chrysin inhibited mRNA expression of PPARα
ER Stress↑, ROS production by chrysin was the critical mediator behind induction of ER stress, leading to JNK phosphorylation, intracellular Ca2+ release, and activation of the mitochondrial apoptosis pathway
Ca+2↑,
ERK↓, reduced protein expression of p-ERK/ERK
MMP↑, Chrysin pretreatment led to an increase in mitochondrial ROS creation, swelling in isolated mitochondria from hepatocytes, collapse in MMP, and release cytochrome c.
Cyt‑c↑,
Casp3↑, Chrysin could elevate caspase-3 activity in the HCC rats group
HK2↓, chrysin declined HK-2 combined with VDAC-1 on mitochondria
NRF2↓, chrysin inhibited the Nrf2 expression and its downstream genes comprising AKR1B10, HO-1, and MRP5 by quenching ERK and PI3K-Akt pathway
HO-1↓,
MMP2↓, Chrysin pretreatment also downregulated MMP2, MMP9, fibronectin, and snail expression
MMP9↓,
Fibronectin↓,
GRP78/BiP↑, chrysin induced GRP78 overexpression, spliced XBP-1, and eIF2-α phosphorylation
XBP-1↓,
p‑eIF2α↑,
*AST↓, Chrysin administration significantly reduced AST, ALT, ALP, LDH and γGT serum activities
ALAT↓,
ALP↓,
LDH↓,
COX2↑, chrysin attenuated COX-2 and NFkB p65 expression, and Bcl-xL and β-arrestin levels
Bcl-xL↓,
IL6↓, Reduction in IL-6 and TNF-α and augmentation in caspases-9 and 3 were observed due to chrysin supplementation.
PGE2↓, Chrysin induced entire suppression NF-kB, COX-2, PG-E2, iNOS as well.
iNOS↓,
DNAdam↑, Chrysin induced apoptosis of cells by causing DNA fragmentation and increasing the proportions of DU145 and PC-3 cells
UPR↑, Also, it induced ER stress via activation of UPR proteins comprising PERK, eIF2α, and GRP78 in DU145 and PC-3 cells.
Hif1a↓, Chrysin increased the ubiquitination and degradation of HIF-1α by increasing its prolyl hydroxylation
EMT↓, chrysin was effective in HeLa cell by inhibiting EMT and CSLC properties, NF-κBp65, and Twist1 expression
Twist↓,
lipid-P↑, Chrysin disrupted intracellular homeostasis by altering MMP, cytosolic Ca (2+) levels, ROS generation, and lipid peroxidation, which plays a role in the death of choriocarcinoma cells.
CLDN1↓, Chrysin decreased CLDN1 and CLDN11 expression in human lung SCC
PDK1↓, Chrysin alleviated p-Akt and inhibited PDK1 and Akt
IL10↓, Chrysin inhibited cytokines release, TNF-α, IL-1β, IL-10, and IL-6 induced by Ni in A549 cells.
TLR4↓, Chrysin suppressed TLR4 and Myd88 mRNA and protein expression.
NOTCH1↑, Chrysin inhibited tumor growth in ATC both in vitro and in vivo through inducing Notch1
PARP↑, Pretreating cells with chrysin increased cleaved PARP, cleaved caspase-3, and declined cyclin D1, Mcl-1, and XIAP.
Mcl-1↓,
XIAP↓,
| - |
Review, |
Park, |
NA |
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- |
Review, |
Stroke, |
NA |
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*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
*memory↑, CA prevented LPS-induced memory impairment and neuronal loss through behavioral tests and histological examination.
*Aβ↓, CA prevented LPS-induced increases in amyloid β (1-42 specific) (Aβ1-42) accumulation, levels of amyloid precursor protein, and neuronal β-secretase 1 (BACE1), as well as the equilibrium cholinergic system in mouse brain.
*BACE↓,
*MAPK↓, CA down-regulated LPS-induced glial overactivation by inhibiting the MAPK and NF-κB pathway
*NF-kB↓,
*NF-kB↓, CA reduced the levels of NF-κB transcriptionally regulated inflammatory mediators and cytokines such as iNOS, cyclooxygenase-2 (COX-2), IL-1β, and TNF-α in both mouse brain and BV2 microglial cells.
*iNOS↓,
*COX2↓,
*IL1β↓,
*TNF-α↓,
*BDNF∅, we found that BDNF, NGF, NT3, and NT4 mRNA expressions of neurotrophic factors exhibited no changes after CA treatment
*MMPs↓, CA also down-regulated the mRNA levels of MMPs in LPS-treated mice, which might provide another clue for the explanation of the anti-amyloidosis effects of CA (
*antiOx↑, Chicoric acid (CA), a natural phenolic acid extracted from chicory and the echinacea (purple coneflower) plant (Echinacea purpurea), has been regarded as a nutraceutical that has powerful antioxidant and antiobesity activities.
*Obesity↓,
*memory↑, CA prevented LPS-induced memory impairment and neuronal loss through behavioral tests and histological examination.
*Aβ↓, CA prevented LPS-induced increases in amyloid β (1-42 specific) (Aβ1-42) accumulation,
*MAPK↓, CA down-regulated LPS-induced glial overactivation by inhibiting the MAPK and NF-κB pathway.
*NF-kB↓,
*iNOS↓, CA reduced the levels of NF-κB transcriptionally regulated inflammatory mediators and cytokines such as iNOS, cyclooxygenase-2 (COX-2), IL-1β, and TNF-α in both mouse brain and BV2 microglial cells.
*COX2↓,
*IL1β↓,
*TNF-α↓,
*NF-kB↓, Chicoric acid supplementation prevents systemic inflammation-induced memory impairment and amyloidogenesis via inhibition of NF-κB.
*antiOx↑, chicoric acid (CA) has been well-documented due to its excellent antioxidant and antiobesity bioactivities.
*Obesity↓,
*NRF2↑, CA could insert into the pocket of Keap1 and up-regulated Nrf2 signaling and, thus, transcriptionally regulate downstream expressions of antioxidant enzymes including HO-1 and NQO-1
*HO-1↑,
*NQO1↑, 80 μM CA resulted in noticeably increasing in the levels of the expressions of HO-1 and NQO-1
*ROS↓, CA reduced LPS-stimulated ROS over-release
*GSH↑, CA directly quenched free radicals or by increased antioxidant enzymes such as GSH, CAT and SOD
*Catalase↑,
*SOD↑,
*ATP↑, Moreover, CA alleviated the reduction of energy molecule ATP
*COX2↓, Previous of our research proved that CA promoted glucosamine-mediated glucose uptake and ihibited the expressions of COX-2 and iNOS
*iNOS↓,
*neuroP↑, CA could be considered a promising nutritional complement in oxidative stress-related neuroinflammation.
| - |
Review, |
Nor, |
NA |
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Review, |
Arthritis, |
NA |
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*antiOx↑, many pharmacological properties such as anti-oxidant, anti-inflammatory, antitumor, antigenotoxic, anti-depressant, hepatoprotective, cardioprotective, and neuroprotective.
*Inflam↓,
*AntiTum↑,
*hepatoP↑,
*cardioP↑,
*neuroP↑,
*NRF2↑, review indicate that saffron and its constituents could induce the Nrf2 signaling pathway leading to its anti-oxidant and therapeutic effects.
*NF-kB↓, ↓Arthritic pain, inflammation, oxidative stress, NF-κB, iNOS, COX-2, IL-6, IL-10, IL-1β, and TNF-α
↑Nrf2 and HO-1
*iNOS↓,
*COX2↓,
*IL6↓,
*IL10↓,
*IL1β↓,
*TNF-α↓,
*HO-1↑,
ROS↑, ↑Cytotoxicity in cancer cells, ROS, oxidative stress, Nrf2, HO-1, NQO1, and NQO2 ↓LDHA, membrane potential, and ATP level in vitro/A549, HepG2, HCT-116, HeLa, and SK-OV-3 cancer cell lines
NQO1↑,
NRF2↑,
HO-1↑,
NQO2↑,
LDHA↓,
ATP↓,
*hepatoP↑, Hepatoprotective effects ↑SOD, CAT, GPx, and Nrf2 ↓ROS
*SOD↑,
*Catalase↑,
*GPx↑,
*NRF2↑,
*ROS↓,
*cardioP↑, ↓Cardioprotective, ER stress, GRP78, CHOP, apoptosis, and miR-34a ↑Nrf2, HO-1, and Sirt1
*ER Stress↓,
*GRP78/BiP↓,
*CHOP↓,
*Apoptosis↓,
*miR-34a↓,
*SIRT1↑,
chemoP↑, chemoprotective-protective effects of crocin is its anti-inflammatory and anti-oxidant functions
| - |
in-vitro, |
Nor, |
RAW264.7 |
|
|
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*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↑,
TumCD↓, Curcumin plays the antitumor effect by directly promoting tumor cell death and reducing tumor cells' invasive ability.
TumCI↓,
*Inflam↓, curcumin has many pharmacological effects, such as anti-inflammation, antioxidation, antitumor, etc.
*antiOx↓,
*AntiTum↓,
NF-kB↓, Curcumin exerts the therapeutic effect mainly by inhibiting the nuclear factor-κB (NF-κB) signal pathway, inhibiting the production of cyclooxygenase-2 (COX-2),
COX2↓,
Casp9↓, promoting the expression of caspase-9, and directly inducing reactive oxygen species (ROS) production in tumor cells.
ROS↑, Curcumin can induce lethal levels of reactive oxygen species (ROS) in tumors
BioAv↑, Curcumin nanoparticles can solve curcumin's shortcomings, such as poor water solubility and high metabolic rate, and can be effectively used in antitumor therapy.
RadioS↑, Figure 1, Curcumin Increases Radiosensitivity of Tumor
ChemoSen↑,
Imm↑,
PhotoS↑, Curcumin Mediates the Antitumor Effect of PDT
sonoS↑, Curcumin Mediates the Antitumor Effect of SDT
5LO↓, down-regulating the activities of cyclooxygenase-2 (COX-2), lipoxygenase (LOX), inducible nitric oxide synthase (iNOS) and so on, reducing the production of proinflammatory cytokines such as IL-2, tumor necrotic factor-α (TNF-α),
iNOS↓,
IL2↓,
TNF-α↓,
Casp9↑, activating intracellular caspase-9 and caspase-3, reducing the expression of p53, inhibiting Bcl2, and promoting the expression of Bax and down-regulating the proportion of Bcl2/Bax
Casp3↑,
Bcl-2↓,
BAX↑,
Apoptosis↑, promote apoptosis by activating caspase-4 and stimulating the Endoplasmic reticulum (ER) stress pathway and mitochondria stress pathway in tumor cells [
ER Stress↑,
cycD1/CCND1↓, It reduces the expression of cyclin D1, cyclin kinase-dependent kinase 2 (CDK2), cdc2/cyclin B complex, and other cell cycle-related proteins,
CDK2↓,
CycB/CCNB1↓,
TumCCA↑, blocks tumor cells from G1 / S phase and G2 / M phase, thus exerting an antitumor effect
MMPs↓, curcumin inhibits tumor invasion and metastasis by inhibiting NF-κB and other signaling pathways, such as chemokine and matrix metalloproteinases (MMPs)
*radioP↑, Curcumin can effectively treat and prevent radiation adverse reactions such as radiation dermatitis and radiation pneumonia by reducing the expression of inflammatory factors such as fibrotic cytokines, TNF-α, and IL-1, inhibiting NF-κB signal pathwa
chemoP↑, Protective Effect of Curcumin on Side Effects of Chemotherapy
hepatoP↑, urcumin alleviates the hepatotoxicity caused by chemotherapy through anti-inflammation and antioxidation, reducing the level of liver fibrosis and blood lipids [
cardioP↑, Using curcumin to reduce the cardiotoxicity of chemotherapy can improve the therapeutic effect of tumors and patients' prognosis and quality of life.
eff↑, Curcumin Enhances the Therapeutic Effect of Immunotherapy
PhotoS↑, it has the potential to be a new photosensitizer
eff↑, Curcumin nanoparticles with functions of relieving hypoxia and consuming GSH could improve the ability of curcumin to induce ROS and promote ROS- mediated tumor cell death
ROS↑,
GSH↓,
TumCG↓, Curcumin can prevent tumor growth, angiogenesis, epithelial–mesenchymal transition, invasion, and metastasis by modulating the expression of tumor-related non-coding RNA (ncRNA)
angioG↓,
EMT↓,
TumCI↓,
TumMeta↓,
*GutMicro↑, curcumin plays a crucial role in regulating the gut microbiota via biotransformation of curcumin and its metabolites.
*BioAv↓, one of the primary drawbacks of taking curcumin alone is its low bioavailability, which appears to be caused by poor absorption, fast metabolism, and excretion
*HO-1↑, Curcumin is an efficient inducer of hemoxygenase-1 and a powerful inhibitor of reactive oxygen-generating enzymes, such as cyclooxygenase (COX), inducible nitric oxygen synthase (iNOS), lipoxygenase, and xanthine dehydrogenase/oxidase
*ROS↓,
*COX2↓,
*iNOS↓,
PKCδ↓, Curcumin is also a powerful inhibitor of protein kinase C (PKC), tyrosine kinase, epidermal growth factor receptor (EGFR), and IB kinase.
EGFR↓,
NF-kB↓, It suppresses NF-κB activation and the expression of oncogenes, such as c-jun, c-fos, c-myc, Akt, PI3K, cyclin-dependent kinase (CDK)
cJun↓,
cFos↓,
cMyc↓,
Akt↓,
PI3K↓,
CDK4↓,
*TNF-α↓, Continuous supplementation with nanocurcumin (two 40 mg capsules/day after a meal) for 3 months suppressed expression of inflammatory tumor necrosis factor-alpha (TNF-α), high sensitive protein with C-reactive protein (CRP), and interleukin-6 (IL-6)
*CRP↓,
*IL6↓,
MMP9↓, curcumin suppressed metastasis to the lung by suppressing NF-κB, MMP-9, COX-2, and vascular endothelial growth factor (VEGF) expression.
VEGF↓,
JAK↓, Curcumin remarkably inhibits JAK/STAT signaling by downregulating pro-inflammatory interleukins, such as IL-1, IL-2, IL-6, IL-8, IL-12, and MCP-1.
STAT↓,
IL1↓,
IL2↓,
IL6↓,
IL8↓,
IL12↓,
MCP1↓,
Apoptosis↑, It promotes apoptosis and ER stress by targeting phosphorylated protein kinase-like ER-resident kinase,
ER Stress↑,
5LO↓, inhibiting lipoxygenase and xanthine oxidase activity
XO↓,
*NRF2↑, The expression of nuclear factors erythroid 2-related factor (Nrf2) and heme oxygenase 1 (HO-1) is boosted by curcumin
*HO-1↑,
*AChE↓, Curcumin also inhibits the key enzyme acetylcholinesterase (AChE) and p300, a positive regulator of the Wnt/β-catenin pathway
*neuroP↑, Curcumin has also been suggested to prevent and cure neurotoxicity by replenishing dopamine and 3,4-dihydroxyphenylacetic acid levels.
*glucose↓, remarkably lowers blood glucose levels and improves insulin resistance by reducing hepatic glucose synthesis, inhibiting inflammatory reactions produced by hyperglycemia,
*GLUT2↑, boosting glucose transporters 2 (GLUT2), 3 (GLUT3), and 4 (GLUT4) gene expression, enhancing glucose uptake, and activating the AMPK signaling pathway.
*GLUT3↑,
*GLUT4↑,
*GlucoseCon↑,
*AMPK↑,
*BMD↑, Supplementation with nanomicelle curcumin (80 mg) alone or in combination with Nigella sativa oil (1000 mg) for 2–6 months increased plasma levels of miRNA-21 in postmenopausal women with low bone mass density.
*MDA↓, (1000 mg/day) for 8 weeks reduced serum levels of malondialdehyde (MDA) and high-sensitivity CRP (hs-CRP) and increased the total antioxidant capacity in 81 healthy postmenopausal women
*eff↑, Loriczova et al. demonstrated that iron (18 mg and 65 mg) supplementation along with curcumin (500 mg) reduces iron-induced systemic inflammation by reducing plasma levels of TNF-α
eff↑, high-dose vitamin C (25–100 g/day) along with oral nutrient supplementation including curcumin (1–3 g/day) had improved QoL and survival
P53↑, Curcumin was also reported to induce p53 and Bax expression in patients with colorectal cancer, causing apoptosis and DNA fragmentation and suppressing TNF-α and Bcl-2.
BAX↑,
DNAdam↑,
Bcl-2↓,
CSCs↓, The combination of curcumin, 5-fluorouracil (5-FU) and oxaliplatin (FOLFOX) in colorectal liver metastases reduced stem cell markers, such as aldehyde dehydrogenase and CD133.
ALDH↓,
CD133↑,
Showing Research Papers: 1 to 50 of 141
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 141
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↓, 1, GSH↓, 3, GSH↑, 1, GSTs↑, 1, HO-1↓, 2, HO-1↑, 4, lipid-P↓, 1, lipid-P↑, 2, MDA↓, 1, MPO↓, 1, NQO1↑, 1, NRF2↓, 1, NRF2↑, 5, ROS↓, 2, ROS↑, 13, ROS⇅, 3, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↑, 1, ATP↓, 1, CDC25↓, 1, MMP↓, 4, MMP↑, 1, MPT↑, 1, XIAP↓, 3,
Core Metabolism/Glycolysis(tgid=4) ⓘ
12LOX↓, 1, ACSL4↑, 1, ALAT↓, 1, ALAT↝, 1, AMPK↓, 1, p‑AMPK↑, 1, cMyc↓, 3, FASN↓, 1, Glycolysis↓, 1, HK2↓, 1, LDH↓, 1, LDHA↓, 1, LDL↓, 1, PDK1↓, 1, PKM2↓, 1, PPARα↓, 1, PPARγ↑, 1, SIRT1↑, 1, TCA↓, 1, Warburg↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 6, p‑Akt↓, 1, APAF1↑, 1, Apoptosis↑, 9, Bak↓, 1, BAX↑, 8, Bax:Bcl2↑, 1, Bcl-2↓, 8, Bcl-xL↓, 1, BID↑, 2, Casp↑, 1, Casp12↑, 1, Casp3↓, 1, Casp3↑, 10, Casp7↑, 2, Casp8↑, 3, Casp9↓, 1, Casp9↑, 7, Cyt‑c↓, 1, Cyt‑c↑, 7, Diablo↑, 1, DR5↑, 2, Fap1↓, 1, Fas↑, 2, hTERT/TERT↓, 1, ICAD↓, 1, iNOS↓, 13, JNK↓, 2, JNK↑, 2, MAPK↓, 2, MAPK↑, 1, Mcl-1↓, 1, p38↓, 1, p38↑, 1, survivin↓, 2, TRPV1↑, 1, TumCD↓, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
HER2/EBBR2↓, 1, SOX9↓, 1, SOX9↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
cJun↓, 1, other↓, 1, other↝, 1, PhotoS↑, 2, sonoS↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↑, 1, p‑eIF2α↑, 1, ER Stress↑, 5, GRP78/BiP↑, 2, HSP27↓, 1, HSP70/HSPA5↑, 1, NQO2↑, 1, UPR↑, 1, XBP-1↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
ATG5↑, 2, Beclin-1↑, 1, BNIP3↑, 1, LC3I↑, 1, LC3II↑, 1, p62↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
CHK1↓, 1, DNAdam↑, 5, P53↑, 9, PARP↑, 2, cl‑PARP↑, 2, PCNA↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
p‑CDK1↓, 1, CDK2↓, 1, CDK4↓, 4, CycB/CCNB1↓, 2, cycD1/CCND1↓, 7, cycE/CCNE↓, 1, cycE/CCNE↑, 2, P21↓, 1, P21↑, 5, p‑RB1↓, 1, TumCCA↑, 6,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ALDH↓, 1, CD133↑, 1, CD44↓, 2, cFos↓, 1, CSCs↓, 3, EMT↓, 2, ERK↓, 3, p‑ERK↓, 2, FGF↓, 1, FOXM1↓, 1, GSK‐3β↓, 1, HDAC↓, 1, IGF-1R↓, 1, mTOR↓, 3, Nanog↓, 1, NOTCH1↑, 1, OCT4↓, 1, PI3K↓, 3, SOX2↓, 1, STAT↓, 1, STAT3↓, 4, TOP1↓, 1, TOP2↓, 1, TumCG↓, 2,
Migration(tgid=13) ⓘ
5LO↓, 2, Ca+2↑, 3, i-Ca+2?, 1, cal2↓, 1, CEA↓, 1, CLDN1↓, 1, E-cadherin↑, 1, p‑FAK↓, 1, Fibronectin↓, 1, MMP-10↓, 1, MMP2↓, 2, MMP9↓, 6, MMPs↓, 1, PKCδ↓, 1, Slug↓, 1, Snail↓, 2, TET1↑, 1, TIMP2↑, 1, TumCI↓, 3, TumCMig↓, 2, TumCP↓, 3, TumMeta↓, 3, Twist↓, 2, Vim↓, 2, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 4, EGFR↓, 2, EGFR↑, 1, Hif1a↓, 7, NO↓, 1, VEGF↓, 10, VEGFR2↓, 1,
Barriers & Transport(tgid=15) ⓘ
P-gp↓, 1, P-gp⇅, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX1↑, 1, COX2↓, 10, COX2↑, 1, CRP↓, 1, IFN-γ↓, 2, IL1↓, 2, IL10↓, 3, IL12↓, 1, IL1β↓, 6, IL2↓, 3, IL4↓, 1, IL6↓, 10, IL8↓, 4, Imm↑, 2, Inflam↓, 3, JAK↓, 1, M1↓, 1, MCP1↓, 1, NF-kB↓, 11, NF-kB↑, 1, PGE2↓, 2, TLR4↓, 1, TNF-α↓, 7,
Synaptic & Neurotransmission(tgid=18) ⓘ
ADAM10?, 1,
Protein Aggregation(tgid=19) ⓘ
XO↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 2, BioEnh↑, 2, ChemoSen↑, 5, Dose↝, 2, Dose∅, 3, eff↓, 1, eff↑, 9, P450↓, 1, RadioS↑, 3, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, ALAT↝, 1, ALP↓, 1, ALP↝, 1, AR↓, 1, AST↝, 1, CEA↓, 1, CRP↓, 1, E6↓, 1, E7↓, 1, EGFR↓, 2, EGFR↑, 1, FOXM1↓, 1, GutMicro↑, 1, HER2/EBBR2↓, 1, hTERT/TERT↓, 1, IL6↓, 10, LDH↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↓, 1, AntiCan↑, 4, AntiTum↑, 1, cardioP↑, 2, chemoP↑, 4, chemoPv↑, 3, cognitive?, 1, hepatoP↑, 2, neuroP↑, 2, RenoP↑, 1, Risk↓, 2,
Total Targets: 245
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiBio↑, 2,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 2, antiOx↑, 16, Catalase↑, 11, Ferroptosis↓, 1, GPx↑, 6, GSH↑, 11, GSR↑, 2, GSTs↑, 2, HDL↑, 1, HO-1↓, 1, HO-1↑, 10, Keap1↓, 2, Keap1↑, 1, lipid-P↓, 7, MDA↓, 11, MPO↓, 4, NOX4↓, 1, NQO1↑, 2, NRF2↑, 17, RNS↓, 1, ROS↓, 25, SOD↑, 18, SOD1↑, 1, TBARS↓, 4, Trx1↑, 1, uricA↓, 1, VitC↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 3, Insulin↑, 1, MEK↓, 1, MMP↑, 2, MMP∅, 1, mtDam↓, 1, mtDam↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
12LOX↓, 1, ACC↑, 1, adiP↑, 1, ALAT↓, 2, AMPK↑, 1, p‑AMPK↑, 1, cAMP↑, 2, glucose↓, 1, glucose↝, 1, GlucoseCon↑, 2, GLUT2↑, 2, H2S↑, 1, HMG-CoA↓, 1, LDH↓, 3, NADPH↑, 1, PPARα↑, 2, PPARγ↑, 2, SIRT1↑, 2,
Cell Death(tgid=5) ⓘ
Akt↓, 2, Akt↑, 1, APAF1↓, 1, Apoptosis↓, 5, BAX↓, 4, Bcl-2↑, 2, Casp1↓, 1, Casp3↓, 5, Casp3∅, 1, Casp6↓, 1, Casp9↓, 4, Cyt‑c↓, 2, Cyt‑c∅, 1, Fas↓, 2, Ferroptosis↓, 1, HGF/c-Met↑, 1, iNOS↓, 39, iNOS↑, 1, JNK↓, 3, p‑JNK↓, 1, MAPK↓, 3, p38↓, 2,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 1, cJun↓, 1, other↑, 1, other↝, 2,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↓, 1, CHOP↑, 1, ER Stress↓, 2, GRP78/BiP↓, 1, GRP78/BiP↑, 1, GRP94↑, 1, HSP70/HSPA5↑, 2,
DNA Damage & Repair(tgid=10) ⓘ
P53↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, ERK↑, 1, p‑ERK↑, 1, GSK‐3β↓, 3, HDAC↓, 1, miR-34a↓, 1, PI3K↓, 2, p‑STAT1↓, 1, p‑STAT3↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, APP↓, 1, Ca+2↓, 1, CLDN1↑, 1, MMP13↓, 1, MMP3↓, 1, MMP9↓, 1, MMPs↓, 1, MUC1↑, 1, VCAM-1↓, 1, ZO-1↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
p‑eNOS↑, 1, Hif1a↓, 1, NO↓, 10, NO↑, 1, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 8, CLDN3↑, 1, GastroP↑, 1, GLUT3↑, 1, GLUT4↑, 1, IBI↑, 1, OCLN↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CB2 / CNR2↑, 3, CD4+↑, 1, COX1↓, 3, COX2↓, 27, CRP↓, 1, ICAM-1↓, 1, IFN-γ↓, 2, IL10↓, 1, IL17↓, 1, IL1β↓, 19, IL2↓, 1, IL6↓, 17, IL6↑, 1, Imm↑, 1, INF-γ↓, 1, Inflam↓, 23, Inflam↑, 1, IκB↑, 1, p‑JAK1↓, 1, p‑JAK2↓, 1, MCP1↓, 1, MIP‑1α↓, 1, NF-kB↓, 21, p‑NF-kB↓, 2, p65↓, 1, PGE2↓, 7, PGE2↑, 1, Th1 response↓, 1, Th2↑, 2, TLR4↓, 5, TNF-α↓, 26,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↑, 1, AChE↓, 7, BChE↓, 3, BDNF↑, 1, BDNF∅, 1, ChAT↑, 2, MAOA↓, 1, tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 1, Aβ↓, 7, BACE↓, 5, NLRP3↓, 2,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
GR↑, 1, RAAS↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 5, BioAv↑, 7, BioAv↝, 4, BioEnh↑, 1, Dose↝, 2, eff↑, 5, Half-Life↓, 1, Half-Life↝, 2,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 2, AST↓, 3, BMD↑, 1, BP↓, 2, creat↓, 2, CRP↓, 1, GutMicro↑, 3, IL6↓, 17, IL6↑, 1, LDH↓, 3,
Functional Outcomes(tgid=23) ⓘ
AntiDiabetic↑, 1, AntiTum↓, 1, AntiTum↑, 2, cardioP↑, 8, cognitive↑, 10, hepatoP↑, 5, memory↑, 11, motorD↑, 2, neuroP↑, 22, NP/CIPN↓, 1, Obesity↓, 2, Pain↓, 2, radioP↑, 1, RenoP↑, 3, toxicity↓, 1, Weight↑, 1, Wound Healing↑, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, Bacteria↓, 2, CD8+↑, 1, Diar↓, 1, Inf↓, 1,
Total Targets: 205
Scientific Paper Hit Count for: iNOS, Inducible nitric oxide synthase
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#:159 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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