BP Cancer Research Results

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3865- ACNs,    Consumption of anthocyanin-rich cherry juice for 12 weeks improves memory and cognition in older adults with mild-to-moderate dementia
- Human, AD, NA
*memory↑, Improvements in verbal fluency (p = 0.014), short-term memory (p = 0.014) and long-term memory (p ≤ 0.001) were found in the cherry juice group.
*BP↓, A significant reduction in systolic (p = 0.038) blood pressure and a trend for diastolic (p = 0.160) blood pressure reduction was evident in the intervention group.
*cognitive↑, This study found that daily consumption of a feasible serving of anthocyanin-rich cherry juice for 12 weeks improved cognitive performance across almost all tasks in older adults with mild-to-moderate dementia

5354- AL,    Therapeutic Potential of Allicin-Rich Garlic Preparations: Emphasis on Clinical Evidence toward Upcoming Drugs Formulation
- Review, Var, NA
*LDL↓, Indeed, clinical studies on healthy subjects have evidenced that standardized garlic treatment (900 mg/day) significantly reduces total cholesterol (TC) and low-density lipoprotein cholesterol (c-LDL).
*antiOx↑, Multiple studies have focused on allicin therapeutic potential as an antioxidant (inducing antioxidant product production),
AntiCan↑, anticancer (triggering cancer cells apoptosis and inhibiting tumor growth),
*cardioP↑, cardioprotective (decreasing angiogenesis and inducing vasorelaxation)
*BP↓, Conversely, aged garlic extract supplementation was shown to be more effective than the placebo in lowering systolic blood pressure
*Weight↓, Garlic powder supplementation (800 mg/daily) resulted in a significant decrease in body weight and body fat mass (
NK cell↑, Actually, aged garlic administration in patients with advanced cancer of the digestive system led to an improvement of natural killer (NK) cell activity but did not cause improvement in QoL
*AntiDiabetic↑, Actually, daily garlic allicin supplementation (0.05–1.5 g) displayed a positive and sustained role in blood glucose, total cholesterol (TC), and high/low density lipoprotein (HDL-c/LDL-c) regulation in type 2 diabetes mellitus (T2DM) management
*GSH↑, 2-month application of coated garlic powder tablets (900 mg with alliin and allicin contents of 1.3% and 0.6%, respectively), the glutathione (GSH) concentration significantly increased in circulating human erythrocytes

2558- AL,    Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment
- Review, AD, NA
*AntiCan↑, Allicin has shown anticancer, antimicrobial, antioxidant properties and also serves as an efficient therapeutic agent against cardiovascular diseases
*antiOx↑,
*cardioP↑,
*neuroP↑, present review describes allicin as an antioxidant, and neuroprotective molecule
cognitive↑, that can ameliorate the cognitive abilities in case of neurodegenerative and neuropsychological disorders.
*ROS↓, As an antioxidant, allicin fights the reactive oxygen species (ROS) by downregulation of NOX (NADPH oxidizing) enzymes, it can directly interact to reduce the cellular levels of different types of ROS produced by a variety of peroxidases.
*NOX↓,
*TLR4↓, inhibition of TLR4/MyD88/NF-κB, P38 and JNK pathways.
*NF-kB↓,
*JNK↓,
*AntiAg↑, A low concentration of allicin (0.4 mM) can inhibit the platelet aggregation up to 90%, the impact is significantly higher than of similar concentration of aspirin.
*H2S↑, Allicin decomposes rapidly and undergoes a series of reactions with glutathione resulting in the production of hydrogen sulphide (H2S).
*BP↓, H2S is a gaseous signalling molecule involved in the regulation of blood pressure.
Telomerase↓, Allicin inhibits the activity of telomerase in a dose dependent manner subsequently inhibiting the proliferation in the cancer cells
*Insulin↑, Studies have shown a significant increase in the blood insulin levels after treatment with allicin
BioAv↝, optimum temperature for the activity of alliinase is 33 °C, it operates best at pH 6.5, the enzyme is sensitive to acids [42,43] (Figure 3), enteric-coated formulations of garlic supplements are therefore recommended
*GSH↑, It helps to lower the hyperglycaemic conditions and improves the glutathione and catalase biosynthesis [37,38]
*Catalase↑,

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↓,

236- AL,    Allicin: Chemistry and Biological Properties
- Analysis, NA, NA
GSH↓, allicin reacts with GSH
Bacteria↓, Antimicrobial
LDL↓, reduction without altering HDL
ROS↑, antioxidant at low doses
NRF2↑,
cognitive↑, by activating the Nrf2-system
memory↑, by activating the Nrf2-system
BP↓, via H2S generation
RNS↓,

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

5574- B-Gluc,    Beta Glucan: Health Benefits in Obesity and Metabolic Syndrome
- Review, Obesity, NA
*BioAv↑, β-glucan is a relatively inexpensive milling byproduct, and it is added to foods on the assumption that this will contribute to health benefits.
*toxicity↓, Moreover, no human adverse effects have been reported following the consumption of a diet rich in β-glucan from oat or barley flour or their extracts [70].
*Imm↑, Among polysaccharides that act as immunostimulants, β-glucans were found to be the most effective against infectious diseases and cancer [88].
*eff↑, The immunological potency of β-glucans varies with the molecular mass, solution conformation, backbone structure, degree of branching as well as the cell type that is targeted [89].
*Risk↓, pretreatment of high-risk surgical patients with intravenous yeast β-(1,3; 1,6)-D-glucan decreased the infection incidence, shortened intensive care unit length stay, and improved survival in comparison to a saline placebo injection
*Weight↓, In this particular study, chitin-glucan decreased high fat diet-induced body weight gain, fat mass development, fasting hyperglycemia, glucose intolerance,
*eff↝, A drink containing 5 g of oat β-glucan with a molecular weight 70 000 Da significantly lowered postprandial glucose and insulin levels relative to a rice drink control, while a similar drink containing barley β-glucan 40 000 Da had no effect
*BP↓, 8 g/day of supplemented soluble fiber from oat bran over 12 weeks significantly reduced both systolic and diastolic blood pressure in comparison to the control [197].
*GutMicro↑, Beta glucans selectively support the growth of Lactobacilli and Bifidobacteria, both of them being antagonists to pathogenic bacteria in the digestive system [
*eff↓, freeze-thaw cycle reduced the solubility of β-glucan in oat bran muffins by 9% to 55% of the fresh values.

3690- BM,    Neurocognitive Effect of Nootropic Drug Brahmi (Bacopa monnieri) in Alzheimer's Disease
- Review, AD, NA
*ROS↓, EBm promotes free radical scavenger mechanisms
*5LO↓, reduces lipoxygenase activity reducing lipid peroxidation, increases glutathione peroxidase and chelates iron.
*lipid-P↓,
*GPx↑,
*IronCh↑,
*neuroP↑, EBm was seen to protect the cholinergic neurons and reduce anticholinesterase activity comparable to donepezil, rivastigmine, and galantamine.
*AChE↓,
*memory↑, EBm improved the total memory score and maximum improvement was seen in logical memory and paired associate learning in humans and reversed phenytoin-induced memory impairment in experimental model.
*toxicity↓, Mild nausea and gastrointestinal upset are seen in humans.
*SOD↑, EBm was administered to the rats for 21 days. It showed increase in activity of enzymes SOD, CAT, and GPx in prefrontal cortex, hippocampus, and striatum. I
*Catalase↑,
*cognitive↑, administration in indicated doses may act as a remedy for age-associated memory and cognitive decline in AD.
*ChAT↑, OBX reduced cholinergic activity and hence also ChAT in hippocampus. Subsequent administration of EBm and tacrine to the substrate, however, reversed this effect
*Ach↑,
*BP↓, Brahmi decreased systolic and diastolic blood pressure without significantly affecting heart rate.

5842- CAP,    Capsaicin: Current Understanding of Its Mechanisms and Therapy of Pain and Other Pre-Clinical and Clinical Uses
- Review, Nor, NA - Review, Diabetic, NA
*Pain↓, capsaicin promotes pain relief when used in the right dosage and frequency.
*TRPV1↑, capsaicin-induced pain is also used to assess new molecules that target TRPV1 receptor. Capsaicin activates TRPV1
AMPK↑, The inhibitory effect of capsaicin on this process seems to involve the activation of 5’ adenosine monophosphate-activated protein kinase (AMPK) in conjunction with intracellular ROS release
ROS↑,
TumCP↑, AMPK activation is also linked to inhibition of cell proliferation and apoptosis [153,154]
Apoptosis↑,
TumCCA↑, capsaicin targets preadipocyte proliferation by blocking the S-phase of the cell cycle [149].
Casp3↑, capsaicin induces apoptosis in preadipocytes via the activation of caspase-3, Bax, and Bak, cleavage of PARP, and down-regulation of Bcl-2
BAX↑,
Bak↑,
cl‑PARP↑,
Bcl-2↓,
RNS↑, capsaicin induces apoptosis in BMSC via increased production of ROS and reactive nitrogen species (RNS) [
*glucose↓, healthy male volunteers revealed that capsaicin lowers glucose and increases insulin levels shortly after oral administration
*Insulin↑,
*BP↓, Capsaicin stimulates the release of CGRP through the activation of TRPV1 and therefore decreases blood pressure
*AntiAg↑, Capsaicin has been shown to inhibit platelet aggregation [199,200], which may also provide protection against cardiovascular diseases
ER Stress↑, endoplasmic reticulum stress in human nasopharyngeal carcinoma and pancreatic cancer cells,
Hif1a↓, capsaicin increases the degradation of hypoxia inducible factor 1α in non-small cell lung cancer,
chemoPv↑, mounting evidence supporting a chemo-preventive role for capsaicin in cancer cell culture and animal models,

6022- CGA,    Chlorogenic Acid: Recent Advances on Its Dual Role as a Food Additive and a Nutraceutical against Metabolic Syndrome
- Review, Nor, NA
*antiOx↑, including anti-oxidant, anti-inflammatory, antilipidemic, antidiabetic, and antihypertensive activities.
*Inflam↓,
*AntiDiabetic↑,
*Obesity↓, chlorogenic acid as a nutraceutical for the prevention and treatment of metabolic syndrome and associated disorders, including in vivo studies, clinical trials, and mechanisms of action
*Wound Healing↑, It was found that chlorogenic acid accelerated wound healing.
*BP↓, Significant reductions of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were observed
*Dose↝, A total of 23 healthy subjects (four men and 19 women) were given water (control) and 400 mg of chlorogenic acid dissolved in 200 mL of low nitrate water.
*ROS↓, the mechanism proposed was that chlorogenic acid scavenges reactive oxygen species (ROS) generated by consumption of high-fat diet, which suppresses the expression of inflammation, and consequently reduces fat accumulation,
*Fas↓, chlorogenic acid supplementation in high-fat diet-induced-obese mice significantly inhibited fatty acid synthase (FAS),
*HMG-CoA↓, As for hypercholesterolemia, chlorogenic acid has been found to inhibit 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR)
*GutMicro↑, high-CGAs coffee (80.8 mg) induced a significant increase in the growth of Bifidobacterium spp. as well as Clostridium coccoides-Eubacterium rectale group, the latter group having also potential to benefit human health.

6002- CGA,    Chlorogenic Acid: A Systematic Review on the Biological Functions, Mechanistic Actions, and Therapeutic Potentials
- Review, Var, NA - Review, Diabetic, NA - Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*neuroP↑, including neuroprotection for neurodegenerative disorders and diabetic peripheral neuropathy, anti-inflammation, anti-oxidation, anti-pathogens, mitigation of cardiovascular disorders,
*Inflam↓,
*antiOx↑,
*cardioP↑, Cardiovascular Protective Effect
*NRF2↑, pivotal antioxidants by activating the Nrf2 pathway
*AMPK↑, It elevates AMPK pathways for the maintenance and restoration of metabolic homeostasis of glucose and lipids.
*SOD↑, figure1
*Catalase↑,
*GSH↑,
*GPx↑,
*ROS↓,
*TNF-α↓,
*IL6↓,
*NF-kB↓,
*COX2↓,
*glucose↓, CGA can attenuate glucose absorption
*TRPC1↓, CGA suppresses the levels of transient receptor potential canonical channel 1 (TRPC1) and decreases ROS and Ca2+, thus mitigating lysophosphatidylcholine (LPC)-induced endothelial injuries
*Ca+2↓,
*HO-1↑, enhancing superoxide dismutase (SOD), and producing NO and heme oxygenase (HO)-1
*NF-kB↓, CGAs can regulate NF-κB and PPARα pathways, lower HIF-1α expression, and suppress cardiac apoptotic signaling, thus executing beneficial effects against cardiac hypertrophy
*PPARα↝,
*Hif1a↓,
*JNK↓, CGA can inhibit NF-κB and JNK pathways, exhibiting cardioprotection
*BP↓, GCE (93 or 185 mg for 4 weeks) could lead to a reduction of 4.7 and 5.6 mmHg in levels of systolic blood pressure (SBP) and a decrease of 3.3 and 3.9 mmHg in levels of diastolic blood pressure (DBP)
*AntiDiabetic↑, CGA has shown its functions in protecting β cells from apoptosis, improving β cell function, facilitating glycemic control, and mitigating DM complications.
*hepatoP↑, CGA can mediate hepatoprotective roles in various pathological conditions of the liver via antioxidant and anti-inflammatory features
*TLR4↓, (1) It can inhibit TLR4-mediated activation of NF-κB, thus suppressing pro-inflammatory responses;
*NRF2↑, (3) it can increase the activity of the Nrf2 pathway
*Casp↓, (4) it can inhibit caspases’ activation to suppress hepatic apoptosis induced by chemicals or toxins.
*neuroP↑, CGA has shown diverse neuroprotective effects on various neuropathological conditions which may be exerted through inhibition of neuroinflammation, reduction in ROS production, prevention of oxidation, and suppression of neuronal apoptosis
*Aβ↓, CGA or extracts containing CGA can inhibit Aβ aggregation-caused cellular injury in SH-SY5Y cells, a neuroblastoma cell line
*LDH↓, CGA increases survival and decreases apoptosis via decreasing activities of lactate dehydrogenase (LDH) and the levels of MDA and raising the levels of SOD and GSH-Px
*MDA↓,
*memory↑, CGA prevents Aβ deposition and neuronal loss and ameliorates learning and memory deterioration in APP/PS2 mice
*AChE↓, CGA inhibits acetylcholinesterase (AChE) activity in rat brains, suggesting its beneficial effect against cognitive impairment
*eff↑, CGA protects against injury caused by cerebral ischemia/reperfusion
EMT↝, It also modulates the epithelial–mesenchymal transition (EMT) process of breast cancer cells by downregulation of N-cadherin and upregulation of E-cadherin
N-cadherin↓,
E-cadherin↑,
TumCCA↑, CGA can stall the cells in the S phase and cause DNA injury in human colon cancer cell lines such as HCT116 and HT29 by increasing ROS production, upregulation of phosphorylated p53, HO-1, and Nrf2
ROS↑,
p‑P53↑,
HO-1↑,
NRF2↑,
ChemoSen↑, CGA in combination with doxorubicin suppresses cellular metabolic activity, colony formation, and cell growth of U2OS and MG-63 cells by upregulating caspase-3 and PARP and suppressing the p44/42 MAPK pathway, thus inducing apoptosis
mtDam↑, mechanism involves CGA-mediated excessive ROS production, causing mitochondrial dysfunction, leading to increases in cleaved levels of caspase-3, caspase-9, PARP, and Bax/Bcl-2 ratio
Casp3↑,
Casp9↑,
PARP↑,
Bax:Bcl2↑,
TumCG↓, in vivo experiments showing that CGA can reduce tumor growth and volume in pancreatic cancer cell-bearing nude mice by modifying cancer cell metabolism through decreasing levels of cyclin D1, c-Myc, and cyclin-dependent kinase-2 (CDK-2),
cycD1/CCND1↓,
cMyc↓,
CDK2↓,
mitResp↓, interrupting mitochondrial respiration, and suppressing aerobic glycolysis
Glycolysis↓,
Hif1a↓, CGA arrests cells at the phase of G1 and inhibits cell viability of prostate cancer cell DU145 by suppressing the levels of HIF-1α and SPHK-1, PCNA, cyclin-D, CDK-4, p-Akt, p-GSK-3β, and VEGF
PCNA↓,
p‑GSK‐3β↓,
VEGF↓,
PI3K↓, inhibition of the PI3K/Akt/mTOR pathway
Akt↓,
mTOR↓,
OS↑, Extending Lifespan in Worms

6013- CGA,    Advances in Pharmacological Properties, Molecular Mechanisms, and Bioavailability Strategies of Chlorogenic Acid in Cardiovascular Diseases Therapy
- Review, CardioV, NA
*BioAv↝, As a dietary component, CGA exhibits moderate oral bioavailability [9], and its molecular structure remains largely intact during oral digestion
*BioAv↝, The composition of gut microbiota plays a critical role in CGA’s metabolism and absorption, producing 11 key metabolites, with the most primary products dihydrocaffeic acid, dihydroferulic acid, and 3-(3-hydroxyphenyl) propionic acid [
*BP↓, eported that CGA lowers blood pressure by relaxing vascular smooth muscle and improving endothelial function
*ROS↓, inhibiting the sources of reactive oxygen species (ROS), such as NADPH oxidase,
*NADPH↓,
*AntiAg↑, he downregulation of thromboxane A2 plays a crucial role in CGA-mediated inhibition of platelet aggregation
*TXA2↓,
*antiOx↑, cCGA exhibited the strongest antioxidant effect, which may be related to improved mitochondrial function [
*cardioP↑, CGA exerts significant cardioprotective effects by modulating multiple signaling pathways.
*Inflam↓, reduce infarct size in MI induced by left anterior descending artery (LAD) ligation in rats. It achieves this by suppressing inflammation and enhancing the activity of antioxidant enzymes, such as SOD and CAT, thereby improving cardiac function
*SOD↑,
*Catalase↑,
*Ferroptosis↓, CGA’s ability to alleviate ferroptosis
*NF-kB↓, inhibiting the NF-κB and JNK signaling pathways, highlighting its cardioprotective potential in a TAC mouse model
*JNK↓,
*NRF2↑, CGA reduces oxidative stress and ROS-induced damage by upregulating the Nrf2/HO-1 pathway, thereby mitigating doxorubicin-induced cardiotoxicity and improving cardiac tissue integrity
*HO-1↑,
*toxicity↓, which are widely used in traditional Chinese medicine [60,61], it is generally considered safe.
*BioAv↓, CGA struggles to cross lipophilic membranes, resulting in poor absorption and bioavailability [69]. Simply increasing the oral dose is not an advisable solution, as it carries significant risks.
*BioAv↑, in vitro study reported that the covalent bonding between CGA and soluble oat β-glucan significantly improved CGA’s structural stability and maximized its pharmacological potential
*BioAv↑, Studies have reported that CGA-loaded liposomes, prepared from cholesterol and phosphatidylcholine, showed a relative oral bioavailability of 129.38% compared to free CGA.
eff↑, bovine serum albumin (BSA)-decorated chlorogenic acid silver nanoparticles (AgNPs-CGA-BSA) exhibited significant antioxidant and anticancer effects both in vitro and in vivo.

6008- CGA,    Risk Assessment of Chlorogenic and Isochlorogenic Acids in Coffee By-Products
- Review, Nor, NA
*toxicity↓, which indicated no significant evidence of toxic or adverse effects following acute oral exposure
*antiOx↑, CQAs have antioxidant [68], antibacterial [69], antiviral [70], antidiabetic [71], neuroprotective [72,73], anti-inflammatory [74], and cytostatic effects [75,76].
*Bacteria↓,
*AntiDiabetic↑,
*neuroP↑, Several in vivo studies have demonstrated the neuroprotective properties of 5-CQA
*Inflam↓,
*cardioP↑, CQAs have been used therapeutically in some clinical treatments as well, e.g., in the treatment of cardiovascular diseases [77] and arterial hypertension (high blood pressure)
*BP↓,
*other↓, CQA (i.g.) in doses of 50–200 mg/kg bw (aluminum chloride (AlCl3), 35 mg/kg bw per day) weakens aluminum-induced Al3+-accumulation, oxidative stress, mitochondrial damage, and nuclear pyknosis in the hippocampus
eff↓, Chlorogenic acid has been found to counteract the effects of metformin, a pharmaceutical drug used to manage elevated blood sugar levels. only observed at high levels of chlorogenic acid, which is unlikely to occur in humans

6089- CHOC,    Cocoa flavanol consumption improves cognitive function, blood pressure control, and metabolic profile in elderly subjects: the Cocoa, Cognition, and Aging (CoCoA) Study—a randomized controlled trial
- Trial, Nor, NA
*Dose↝, consume daily for 8 wk a drink containing 993 mg [high flavanol (HF)], 520 mg [intermediate flavanol (IF)], or 48 mg [low flavanol (LF)] cocoa flavanols (CFs).
*BP↓, Significantly different improvements in insulin resistance (P < 0.0001), blood pressure (P < 0.0001), and lipid peroxidation (P = 0.001) were also observed for the HF and IF groups in comparison with the LF group.
*cognitive↑, This dietary intervention study provides evidence that regular CF consumption can reduce some measures of age-related cognitive dysfunction, possibly through an improvement in insulin sensitivity

6087- CHOC,    Effect of cocoa flavanol supplementation for the prevention of cardiovascular disease events: the COcoa Supplement and Multivitamin Outcomes Study (COSMOS) randomized clinical trial
- Trial, Nor, NA
*cardioP↑, Cocoa extract supplementation did not significantly reduce total cardiovascular events among older adults but reduced CVD death by 27%.
*Dose↝, Participants were randomly assigned to a cocoa extract supplement [500 mg flavanols/d, including 80 mg (–)-epicatechin] or placebo.
*BP↓, Data have shown improvements in endothelium-dependent vasodilation (21–24), blood pressure (BP) (21, 25–27), inflammation (28, 29), and platelet activation (30, 31),
*Inflam↓,
*AntiAg↑,
*Risk↓, In the European Prospective Investigation into Cancer (EPIC)–Norfolk cohort, 15.6 g/d of chocolate intake compared with no intake was significantly associated with a 14% reduction in incident CVD

6086- CHOC,    Cocoa and Chocolate in Human Health and Disease
- Review, Var, NA
*antiOx↑, Antioxidant effects of cocoa may directly influence insulin resistance and, in turn, reduce risk for diabetes.
*AntiDiabetic↑,
*cognitive↑, beneficial effects on satiety, cognitive function, and mood.
*AntiAg↑, Bordeaux and colleagues found that, among healthy participants in a platelet function study, those who had consumed chocolate before testing (n=141) had reduced platelet activity compared to nonconsumers.
*AntiAg↑, dark chocolate consumption decreased platelet adhesion 2 h after consumption in 22 heart transplant patients
*LDL↓, ll three significantly improved LDL and HDL levels from baseline in subjects with high LDL at the start of the study.
*HDL↑, in another trial, HDL increased by 11.4% and 13.7% when subjects consumed dark chocolate and polyphenol-enriched dark chocolate
*BP↓, A relationship between cocoa consumption and reduced BP was first observed in the Zutphen Elderly Study. A 2010 study found that a daily dose of 1052 mg cocoa flavanols was required to reduce 24-h ambulatory BP
*eff↓, Rimbach et al. noted that beneficial effects on BP, FMD, and platelet aggregation have not been found in all human trials (67, 73). Further, improvements are often small when they are observed
*ROS↓, Cocoa intake increases serum antioxidant capacity, protecting the endothelium from oxidative stress and endogenous ROS

6084- CHOC,    Cocoa Polyphenols and Their Potential Benefits for Human Health
- Review, Nor, NA - Review, Stroke, NA - Review, IBD, NA
*lipid-P↓, inhibition of lipid peroxidation and the protection of LDL-cholesterol against oxidation, and increase resistance to oxidative stress.
*ROS↓,
*Inflam↓, decreasing platelet function and inflammation along with diastolic and systolic arterial pressures, which, taken together, may reduce the risk of cardiovascular mortality.
*BP↓,
*cardioP↑, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*chemoPv↑, They also have antiproliferative, antimutagenic, and chemoprotective effects, in addition to their anticariogenic effects.
*BioAv⇅, great controversy surrounding the bioavailability of phenolics in general and of cocoa derivatives in particular.
*antiOx↑, Cocoa has more phenolics and higher antioxidant capacity than green tea, black tea, or red wine
*Risk↓, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*5LO↓, cocoa polyphenols decrease the plasma concentration of proinflammatory cysteinyl leukotrienes through inhibition of 5-LOX, as demonstrated by Sies et al.
*AntiAg↑, Moreover, cocoa decreases not only platelet aggregation, but also adhesion. 234 mg cocoa phenolics a day for 28 days
*Imm↑, Kenny et al. [21] demonstrated that cocoa oligomers are potent stimulators of both the innate immune system and early events in adaptive immunity.
*NF-kB↓, nd their dimeric forms were found to inhibit the NF-κB activation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in T cells,
*other↓, in vivo and in vitro models have provided evidence that pure polyphenols and natural polyphenol plant extracts can modulate intestinal inflammation.
CYP1A1↓, polyphenol cocoa extract leads to the induction of CYP1A1 in breast cancer cells.
COX2↓, hey also inhibited the expression of COX-2,
*Obesity↓, Ferrazzano et al. hypothesized that the polyphenols contained in cocoa may have antiobesity effects due to their ability to suppress fatty acid synthesis while stimulating cell energy expenditure in the mitochondria
*cognitive↑, Moreover, cocoa consumption may also have beneficial effects on satiety, cognitive function, and mood [93].

6094- CHOC,    Impact of Cocoa Products Intake on Plasma and Urine Metabolites: A Review of Targeted and Non-Targeted Studies in Humans
- Human, Nor, NA
*GutMicro↑, polyphenol consumption from cocoa products might change the gut microbiota, exerting prebiotic effects, and which could be related to the activation of anti-inflammatory pathways with benefits in the host and alter the obtained profile of metabolites
*BP↓, as well as improvement in blood pressure, maintenance of normal endothelium-dependent vasodilation, vascular and platelet function
*AntiAg↑,

6098- Chol,    Choline
- Review, Nor, NA - Review, AD, NA
*BioAv↝, Humans can produce choline endogenously in the liver, mostly as phosphatidylcholine, but the amount that the body naturally synthesizes is not sufficient to meet human needs [4]. As a result, humans must obtain some choline from the diet.
*Dose↝, Adequate Intake: 19+ years male:550 mg/day female:425 mg/day Most people in the United States consume less than the AI for choline.
*cardioP↑, Some researchers have suggested that choline might protect cardiovascular health by reducing blood pressure, altering lipid profiles, and reducing levels of plasma homocysteine [3]
*BP↓,
*cognitive↑, People with Alzheimer’s disease have lower levels of the enzyme that converts choline into acetylcholine in the brain [38]. In addition, because phosphatidylcholine can serve as a phospholipid precursor, it might help support the structural integrity
*memory↑, questionnaires from 1991 to 1995 and again from 1998 to 2001 found that those with higher choline intakes had better verbal memory and visual memory [40].
eff∅, choline supplements did not result in clear improvements in cognition in healthy adults [8].

3994- CoQ10,  Se,    Coenzyme Q10 Supplementation in Aging and Disease
- Review, AD, NA - Review, Park, NA
*AntiAge↑, supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics.
*cardioP↑, Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ10
*Inflam↓, Administration of CoQ10 in doses ranging from 60 to 500 mg/day for a 1-week to 4-month intervention period significantly decreased production of inflammatory cytokines
*antiOx↑,
*lipid-P↓, The concentrations of CoQ10 in the plasma of elderly people are positively correlated with levels of physical activity and cholesterol concentrations (Del Pozo-Cruz et al., 2014a,b), as well as with lower lipid oxidative damage.
*QoL↑, Older individuals given a combination of selenium and CoQ10 over a 4-year period reported an improvement in vitality, physical performance, and quality of life
*neuroP↑, health benefits in elderly people by preventing chronic oxidative stress associated with cardiovascular and neurodegenerative diseases
*Dose↝, the highest dose for CoQ10 supplementation is 1200 mg daily according to well-designed randomized, controlled human trials, although doses as high as 3000 mg/day have been used in shorter clinical trials
*BP↓, These authors interpreted the results to indicate a significant reduction in systolic blood pressure without improvements in other CVD risk factors, such as diastolic blood pressure, total cholesterol, LDL- and high-density lipoprotein (HDL)-choleste
*IGF-1↑, elderly healthy participants who received selenium and CoQ10 supplementation for over 4 years, an increase in insulin-like growth factor 1 (IGF-1) and postprandial insulin-like growth factor-binding protein 1 (IGFBP-1) levels
*IGFBP1↑,
*eff↑, A combination of CoQ10 with red yeast rice, berberina, policosanol, astaxanthin, and folic acid significantly decreased total cholesterol, LDL-cholesterol, triglycerides, and glucose in the blood while increasing HDL-cholesterol levels
*LDL↓,
*HDL↑,
*eff↑, 60 patients suffering from statin-associated myopathy were enrolled in a 3-month study to test for efficacy of CoQ10 and selenium treatment. A consistent reduction in their symptoms, including muscle pain, weakness, cramps, and fatigue was observed
*other↑, Because of its capacity to reduce the side-effects of statins, CoQ10 has been proposed to prevent and/or slow the progression of frailty and sarcopenia in the elderly chronically treated with statins.
*RenoP↑, experiments performed on rats showed a promising protective effect of ubiquinol in the kidneys
*ROS↓, 65 patients undergoing hemodialysis, supplementation with high amounts of CoQ10 (1200 mg/day) lowered F2-isoprostane plasma levels indicative of a reduction in oxidative stress
*TNF-α↓, low grade inflammation, respond well to CoQ10 supplementation with significant decrease in TNF-α plasma levels without having an effect on C-reactive protein and IL-6 production
*IL6↓, Another study reported that CoQ10 therapy in doses ranging from 60 to 300 mg/day caused no significant decrease in C-reactive protein while eliciting a significant reduction in IL-6 levels
*other↝, Preclinical studies demonstrated that CoQ can preserve mitochondrial function and reduce the loss of dopaminergic neurons in the case of Parkinson's disease
*other∅, There was no improvement observed in oxidative stress or neurodegeneration markers in a randomized clinical trial in Alzheimer's Disease patients with CoQ10 supplementation at a dose of 400 mg/day for 16 weeks

5780- CRMs,  HCAs,  RES,  Sper,  ASA  Caloric Restriction Mimetics against Age-Associated Disease: Targets, Mechanisms, and Therapeutic Potential
- Review, Var, NA
*OS↑, The permanent or periodic reduction of calorie intake without malnutrition (caloric restriction and fasting) is the only strategy that reliably extends healthspan in mammals including non-human primates.
*AntiAge↑, CRMs will become part of the pharmacological armamentarium against aging and age-related cardiovascular, neurodegenerative, and malignant diseases.
*cardioP↑,
*neuroP↑,
AntiCan↑,
*TNF-α↓, In healthy humans, CR also decreases the levels of circulating tumor necrosis factor-α
*Weight↓, In obese humans, CR promotes significant weight loss and improves general health
*BP↓, Figure 1
*Inflam↓,
*Insulin↓,
*ROS↓,
*AMPK↑,
*mTOR↓,
*SIRT1↑, Resveratrol and Other SIRT1 Activators
CRM↑, Figure2: HCA, Resveratrol, Spermidine, Aspirin, Berberine, EGCG, QC, etc

5071- dietSTF,    Unraveling the impact of intermittent fasting in cancer prevention, mitigation, and treatment: A narrative review
- Review, Var, NA - Review, AD, NA
Risk↓, Intermittent fasting (IF) has emerged as a potential adjunctive strategy in cancer prevention, mitigation, and treatment.
TumCMig↓,
IGF-1↓, IF may reduce cancer risk, including its effects on insulin-like growth factor 1 suppression, autophagy induction, and chronic inflammation reduction.
TumAuto↑,
Inflam↓, IF has been shown to reduce chronic inflammation,13,40 a risk factor for various cancers
ChemoSen↑, we discuss IF’s potential to enhance the efficacy of conventional cancer therapies by sensitizing cancer cells, promoting apoptosis, and reducing treatment-related side effects.
Apoptosis↑,
chemoP↑, IF has shown potential in protecting healthy tissues during chemotherapy.
*glucose↓, Fasting has been shown to enhance metabolic health by improving insulin sensitivity, lowering blood sugar levels, and reducing the risk of type 2 diabetes.
*AntiDiabetic↑,
*cardioP↑, Recent studies support the cardioprotective effect of IF by reducing cholesterol levels, lowering blood pressure, and improving cardiovascular health
*LDL↓,
*BP↓,
*neuroP↑, IF may reduce the risk of neurodegenerative diseases, enhance cognitive function, and improve memory
*cognitive↑,
*memory↑,
*OS↑, some studies have suggested that IF may extend lifespan and improve overall health
*QoL↑,
Imm↑, In the context of cancer prevention, IF may directly affect the function of immune cells, reducing their production of inflammatory cytokines and promoting a more anti-inflammatory environment.5
TumCG↓, Evidence suggests that FMDs can effectively slow tumor growth by altering cancer cell metabolism, enhance the efficacy of traditional cancer therapies by reducing side effects, and potentially bolster antitumor immune surveillance
ChemoSideEff↓, IF may also help alleviate common side effects such as fatigue, nausea, and weight loss associated with cancer treatments
QoL↑, Results showed that chemotherapy-induced QoL decline was significantly less pronounced during fasting periods compared to non-fasting periods

3769- H2S,    Research progress of hydrogen sulfide in Alzheimer's disease from laboratory to hospital: a narrative review
- Review, AD, NA
*APP↓, prevent the progress of the disease by affecting the amyloid precursor protein metabolism, anti-apoptosis, anti-inflammatory, and antioxidant pathways.
*Apoptosis↓,
*Inflam↓,
*antiOx↑,
*BP↓, H2S activates adenosine triphosphate-sensitive potassium channels, which in turn dilates blood vessels and lowers blood pressure, while improving myocardial ischemia-reperfusion injury
*NLRP3↓, activation of NLRP3 inflammatory bodies was inhibited
*ROS↓, catalase may be a key enzyme in the metabolism of H2S, which can convert H2S into sulfide, thereby achieving scavenging effect.
*Aβ↓, H2S can promote APP's non-amyloid metabolic pathway and reduce Aβ production.
*ER Stress↓, H2S may up-regulate brain-derived neurotrophic factor-TrkB pathway to suppress the stress of the endoplasmic reticulum,

4011- K+,    Sodium and potassium intakes among US adults: NHANES 2003–2008
- Analysis, NA, NA
*Dose↓, Overall, <2% of US adults and ∼5% of US men consumed ≥4700 mg K/d (ie, met recommendations for potassium).
*eff↑, potassium intake increases urinary excretion of sodium through action on the renal tubule
*BP↓, potassium intake of ≥4700 mg/d in adults optimally decreases the blood pressure response to sodium intake

3264- Lyco,    Pharmacological potentials of lycopene against aging and aging‐related disorders: A review
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
*antiOx↑, Anti‐oxidative mechanism of lycopene
*ROS↓, Lycopene inhibits ROS generation and subsequent oxidative stress by inducing antioxidant enzymes (SOD, CAT, GSH, GSH‐Px, and GST) and limiting MDA level and lipid peroxidation (LPO).
*SOD↑,
*Catalase↑,
*GSH↑,
*GSTs↑,
*MDA↓,
*lipid-P↓,
*NRF2↑, Lycopene also prevents ROS release by upregulating Nrf2‐mediated HO‐1 levels and inhibiting iNOS‐activated NO generation
*HO-1↑,
*iNOS↓,
*NO↓,
*TAC↑, upregulating total antioxidant capacity (TAC) and direct inhibition of 8‐OHdG, NOX4.
*NOX4↓,
*Inflam↓, Anti‐inflammatory mechanism of lycopene.
*IL1↓, IL‐1, IL‐6, IL‐8, IL‐1β, and TNF‐α release.
*IL6↓,
*IL8↓,
*IL1β↓,
*TNF-α↓,
*TLR2↓, prevents inflammation by inhibiting toll‐like receptors TLR2 and TLR4 and endothelial adhesion molecules VCAM1 and ICAM‐1.
*TLR4↓,
*VCAM-1↓,
*ICAM-1↓,
*STAT3↓, inhibiting STAT3, NF‐κB, ERK pathway, and IL‐6 and TNF‐α release.
*NF-kB↓,
*ERK↓,
*BP↓, Another clinical study demonstrated that consumption of raw tomato (200 g/day) could prevent type 2 diabetes‐associated cardiovascular diseases by lowering systolic and diastolic blood pressure, upregulating ApoA1, and downregulating ApoB levels
ROS↓, lycopene suppresses the metastasis of the SK‐HEP‐1 cell line by NOX‐4 mRNA expression inhibition and the reactive ROS intracellular activity inhibition
PGE2↓, Lycopene is also used to treat colorectal cancer cells in humans, and the introduction of lycopene decreases the prostaglandin E2 and nitric oxide levels
cardioP↑, Lycopene‐rich foods can be highly beneficial in preventing cardiovascular diseases as lycopene is a potential source of antioxidants
*neuroP↑, beneficial role of lycopene on aging‐related neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, has been confirmed in both experimental and clinical trials
*creat↓, Several pre‐clinical studies reported that lycopene treatment significantly reduced serum urea and serum creatinine, as well as reversed various toxic chemical‐induced nephrotoxicity and oxidative damage by exhibiting excellent antioxidative properti
*RenoP↑,
*CRM↑, its potency in treating aging disorders and its role as a mimic of caloric restriction.

1710- Lyco,    Lycopene: A Natural Arsenal in the War against Oxidative Stress and Cardiovascular Diseases
- Review, CardioV, NA
antiOx↓, Lycopene is a potent antioxidant that fights ROS and, subsequently, complications.
ROS↓,
BP↓, It reduces blood pressure via inhibiting the angiotensin-converting enzyme and regulating nitrous oxide bioavailability.
LDL↓, important role in lowering of LDL (low-density lipoproteins) and improving HDL (high-density lipoproteins) levels to minimize atherosclerosis
*toxicity∅, Lycopene is a natural substance that may be used in high doses as a dietary supplement without causing harm to human health or physiology
eff↑, Thermal food processing, particularly in the presence of cooking oils, causes lycopene to micellize and enhance its intestinal absorption rate by a factor of ten
ROS↑, As a pro-oxidant, lycopene may have both good and negative impacts in biological systems, as well as influence the course of human illnesses.
*Half-Life↑, Plasma lycopene has a half-life of 12–33 days in the human body
*BioAv↓, Tomato lycopene is not easily absorbed since it is integrated into the nutritional matrix.
*BioAv↑, Clinical research demonstrates that heat-processed tomato products absorb lycopene more quickly than raw sources, and that adding oil increases absorption
*antiOx↑, Lycopene’s ability to protect against oxidative stress has been established

4801- Lyco,    Lycopene in the Prevention of Cardiovascular Diseases
- Review, CardioV, NA
*BioAv↝, Taking into account the fact that humans are not able to synthesize lycopene de novo, therefore its supply with food is necessary to take advantage of its pro-health properties.
*cardioP↑, protective effect on cardiovascular diseases
*BioAv↑, It is assumed that thanks to the cis form, lycopene is highly bioavailable in the human diet
*BioAv↑, bioavailability of lycopene as a result of its trans to cis isomerization can be achieved by adding fish oil or olive oil to tomato dishes.
*antiOx↑, Antioxidant Effects of Lycopene
*ROS↓, Lycopene is a highly effective antioxidant that, due to the high reactivity between the long polyene chain and free radicals, enables the elimination of singlet oxygen and the reduction of reactive oxygen species (ROS)
*ARE↑, activating the antioxidant response element (ARE)
*SOD↑, it increases the amount of antioxidant enzymes, which include superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px)
*Catalase↑,
*GPx↑,
*lipid-P↓, figure 3
*COX2↓, lycopene (in the form of watermelon powder) reduced inflammation by reducing the activity of the pro-inflammatory mediator cyclooxygenase 2 (COX-2),
*Inflam↓, Anti-Inflammatory Mechanism of Lycopene
*IL1β↓, inhibits the synthesis and release of pro-inflammatory cytokines, including IL-1β, IL-6, IL-8, and TNF-α.
*IL6↓,
*IL8↑,
*TNF-α↓,
*NF-kB↓, inhibition of the nuclear factor κB (NF-κB)
*BP↓, 15 or 30 mg of lycopene was associated with a significant reduction in systolic BP

1659- PBG,    Improvement of insulin resistance, blood pressure and interstitial pH in early developmental stage of insulin resistance in OLETF rats by intake of propolis extracts
- in-vivo, Nor, NA
pH↑, found that interstitial fluid pH in ascites, liver, and skeletal muscle was higher in rats fed propolis diet than rats fed normal diet.
BP↓, Propolis significantly reduced systolic arterial pressures in both 0.1% and 0.5%-propolis contained diet groups compared with normal diet (p < 0.05)
BG↓, decreased levels of blood glucose and plasma insulin

3595- PI,    Black pepper and health claims: a comprehensive treatise
- Review, Var, NA - Review, AD, NA
*antiOx↑, Black pepper (Piper Nigrum L.) is an important healthy food owing to its antioxidant, antimicrobial potential and gastro-protective modules
*ROS↓, The free-radical scavenging activity of black pepper and its active ingredients might be helpful in chemoprevention and controlling progression of tumor growth.
*chemoP↑,
TumCG↓,
*cognitive↑, piperine assist in cognitive brain functioning, boost nutrient's absorption and improve gastrointestinal functionality
*MMPs↓, They postulated that inhibition of interlukon, matrix metalloproteinase, prostaglandin E2, and activator protein 1 are possible routes for their said properties
*PGE2↓,
*AP-1↓,
*5LO↓, Piperine along with some other components can inhibit the expression of enzymes like 5-lipoxygenase and COX-1 that are responsible for leukotriene and prostaglandin biosynthesis.
*COX1↓,
*other↑, It is widely accepted that black pepper is instrumental to prevent and cure gastrointestinal problems. The black pepper enhances the production of hydrochloric acid from stomach thus improving digestion through stimulation of histamine H2 recepto
*other↑, black pepper has diaphoretic (promotes sweating), and diuretic (promotes urination) properties
*other↑, Moreover, it protects intestinal membranes from gastric secretions and ROS damage owing to antioxidant potential.
*SOD↑, black pepper significantly enhanced the activities of antioxidant enzymes, that is, SOD, CAT, GR, and GST.
*Catalase↑,
*GSTs↑,
*GSR↑,
*other↑, black pepper and its active ingredients improve expression of some digestive enzymes along with increase in the secretion of saliva
*Weight↓, piperine intake may decrease body weight
*BioEnh↑, The black pepper and piperine improve the bioavailability of many drugs.
*BioAv↑, Piperine also boosts the bioavailability of important phyto- chemicals contained in other foods, for example, bioactive com- ponents present in curcumin and green tea
*eff↑, The combination of piperine (2.5 mg/kg, i.p., 21 days) with curcumin (20 and 40 mg/kg, i.p., 21 days) showed improved anti-immobility, neurotransmitter enhancing, and monoamine oxidase inhibitory (MAO-A) effects of curcumin
*CYP3A2↓, combination of curcumin and piperine is most likely to inhibit CYP3A, CYP2C9, UGT, and SULT metabolism within the intestinal mucosa (Volak et al., 2008)
*neuroP↑, Neuroprotective Potential of Black Pepper
*BP↓, Piperine (20 mg/kg/day) decreased the blood pressure caused by the blockage of voltage-dependent calcium channels
*other↑, black pepper oil is one of the strongest appetizer; inhalation stimulates the swallowing in post stroke patients with dysphagia.

3916- PS,    The effect of soybean-derived phosphatidylserine on cognitive performance in elderly with subjective memory complaints: a pilot study
- Human, AD, NA
*memory↑, SB-PS supplementation significantly increased the following cognitive parameters: memory recognition (P = 0.004), memory recall (P = 0.006), executive functions (P = 0.004), and mental flexibility (P = 0.01)
*cognitive↑,
*BP↓, Unexpected results from the safety tests suggested that SB-PS significantly reduces both systolic (P = 0.043) and diastolic (P = 0.003) blood pressure
*Dose↝, In order to avoid the influence of PS degradation, Kato-Kataoka et al sent a portion of the capsules to the subjects every single month and instructed the participants to keep the samples under refrigerated conditions.
*eff↑, Powder PS is more stable than liquid, a point that could explain the positive efficacy that Schreiber et al demonstrated in their trial.

3929- PTS,    New Insights into Dietary Pterostilbene: Sources, Metabolism, and Health Promotion Effects
- Review, Var, NA - Review, Arthritis, NA
*NRF2↑, PTS activates the Nrf2 pathway,
*BioAv↑, , PTS has been documented to exhibit an increased bioavailability compared to other stilbene compounds
*ROS↓, Various evidence has demonstrated the effect of PTS in countering oxidative damage and inflammation, imparting preventive and therapeutic benefits in experimental disease models
*Inflam↓,
*HO-1↑, major downstream targets activated following PTS administration were antioxidative enzymes, including HO 1, SOD, catalase, and GPX
*SOD↑,
*Catalase↑,
*GPx↑,
*lipid-P↓, reducing lipid peroxidation in STZ-induced diabetic mice.
*hepatoP↑, figure 4
*neuroP↑,
*iNOS↓, PTS inhibited the transcriptional expression of augmented iNOS levels and moderated the inhibition of COX-2 in a concentration-dependent manner
*COX2↓,
TumMeta↓, PTS in combination with quercetin at 20 mg/kg/day inhibited the metastatic activity in B16-F10 melanoma by reducing the adhesion of B16-F10 cells to the endothelium and also downregulated the levels of Bcl-2 in cancerous cells
SOD2↓, PTS was identified to reduce HCC proliferation through a reduction in SOD2 and the induction of ROS-mediated mitochondrial apoptotic pathways
ROS↑,
TumCI↓, PTS was reported to suppress the invasion and growth of HCC by down-regulating the expression of Metastasis-Associated Protein 1 (MTA1) and histone deacetylase 1 (HDAC1) while upregulating the acetylation of the tumor suppressor protein PTEN
TumCG↓,
HDAC1↓,
PTEN↑,
BP↓, highly purified trans-PTS patented by Chromadex, Irvine, CA, has been proven to significantly reduce blood pressure in adults
*GutMicro↑, PTS significantly reduced paw swelling, the arthritic score, and body weight. Interestingly, it also helped restore the healthy gut microbiota ecosystem by reducing the relative abundance of Helicobacter, Desulfovibrio, Lachnospiraceae, and Mucispiri

3923- PTS,    Pterostilbene Supplement Benefits: Longevity Miracle or Hoax
- Review, AD, NA
*BioAv↑, 80% bioavailability versus 20% for resveratrol
*Half-Life↑, half-life of pterostilbene? 105 minutes. Compare that to resveratrol, which is just 14 minutes
*BBB↑, Just like alpha lipoic acid, pterostilbene has been found to cross the blood brain barrier, which means it might offer protective assistance for neurodegenerative diseases like Alzheimer’s disease and cognitive decline from other oxidative stress con
*BP↓, May reduce blood pressure
*cognitive↑, May slow age-related cognitive decline

3601- QC,    Overviews of Biological Importance of Quercetin: A Bioactive Flavonoid
- Review, Var, NA - Review, AD, NA
*Inflam↓, known for its anti-inflammatory, antihypertensive, vasodilator effects, antiobesity, antihypercholesterolemic and antiatherosclerotic activities
*cardioP↑, beneficial effects include cardiovascular protection, anticancer, antitumor, anti-ulcer, anti-allergy, anti-viral, anti-inflammatory activity, anti-diabetic, gastroprotective effects, antihypertensive, immunomodulatory, and anti-infective.
AntiCan↑,
AntiTum↑,
*neuroP↑, The consumption of flavonoids rich food limits neurodegeneration and to reverse age-dependent loss in cognitive performance.
*cognitive↑,
*ROS↓, It is known to protect brain cells against the oxidative stress, which damages tissue leading to Alzheimer and other neurological conditions
*BP↓, Quercetin supplementation (150 mg/day) reduced systolic blood pressure and plasma oxidized LDL concentrations in overweight subjects
*LDL↓,

3347- QC,    Recent Advances in Potential Health Benefits of Quercetin
- Review, Var, NA - Review, AD, NA
*antiOx↑, Its strong antioxidant properties enable it to scavenge free radicals, reduce oxidative stress, and protect against cellular damage.
*ROS↓,
*Inflam↓, Quercetin’s anti-inflammatory properties involve inhibiting the production of inflammatory cytokines and enzymes,
TumCP↓, exhibits anticancer effects by inhibiting cancer cell proliferation and inducing apoptosis.
Apoptosis↑,
*cardioP↑, cardiovascular benefits such as lowering blood pressure, reducing cholesterol levels, and improving endothelial function
*BP↓, Quercetin‘s ability to reduce blood pressure was also supported by a different investigation
TumMeta↓, The most important impact of quercetin is its ability to inhibit the spread of certain cancers including those of the breast, cervical, lung, colon, prostate, and liver
MDR1↓, quercetin decreased the expression of genes multidrug resistance protein 1 and NAD(P)H quinone oxidoreductase 1 and sensitized MCF-7 cells to the chemotherapy medication doxorubicin
NADPH↓,
ChemoSen↑,
MMPs↓, Inhibiting CT26 cells’ migration and invasion abilities by inhibiting their expression of tissue inhibitors of metalloproteinases (TIMPs) inhibits their invasion and migration abilities
TIMP2↑,
*NLRP3↓, inhibited NLRP3 by acting on this inflammasome
*IFN-γ↑, quercetin significantly upregulates the gene expression and production of interferon-γ (IFN-γ), which is obtained from T helper cell 1 (Th1), and downregulates IL-4, which is obtained from Th2.
*COX2↓, quercetin is known to decrease the production of inflammatory molecules COX-2, nuclear factor-kappa B (NF-κB), activator protein 1 (AP-1), mitogen-activated protein kinase (MAPK), reactive nitric oxide synthase (NOS), and reactive C-protein (CRP)
*NF-kB↓,
*MAPK↓,
*CRP↓,
*IL6↓, Quercetin suppressed the production of inflammatory cytokines such as IL-6, TNF-α, and IL-1β via upregulating TLR4.
*TNF-α↓,
*IL1β↓,
*TLR4↑,
*PKCδ↓, Quercetin employed suppression on the phosphorylation of PKCδ to control the PKCδ–JNK1/2–c-Jun pathway.
*AP-1↓, This pathway arrested the accumulation of AP-1 transcription factor in the target genes, thereby resulting in reduced ICAM-1 and inflammatory inhabitation
*ICAM-1↓,
*NRF2↑, Quercetin overexpressed Nrf2 and targeted its downstream gene, contributing to increased HO-1 levels responsible for the down-regulation of TNF-α, iNOS, and IL-6
*HO-1↑,
*lipid-P↓, Quercetin acts as a potent antioxidant by scavenging ROS, inhibiting lipid peroxidation, and enhancing the activity of antioxidant enzymes
*neuroP↑, This helps to counteract oxidative stress and protect against neurodegenerative processes that contribute to AD
*eff↑, rats treated with chronic rotenone or 3-nitropropionic acid showed enhanced neuroprotection when quercetin and fish oil were taken orally
*memory↑, Both memory and learning abilities in the test animals increased
*cognitive↑,
*AChE↓, The increase in AChE activity brought on by diabetes was prevented in the cerebral cortex and hippocampus by quercetin at a level of 50 mg/kg body weight.
*BioAv↑, consumption of fried onions compared to black tea, suggesting that the form of quercetin present in onions is better absorbed than that in tea
*BioAv↑, This suggests that dietary fat can increase the absorption of quercetin [180]
*BioAv↑, potential of liposomes to enhance the bioactivity and bioavailability of quercetin has been the subject of several investigations
*BioAv↑, several emulsion types that may be employed to encapsulate quercetin, but oil-in-water (O/W) emulsions are the most widely utilized.
*BioAv↑, the kind of oil (triglyceride oils made up of either long-chain or medium-chain fatty acids) affected the bioaccessibility of quercetin and gastrointestinal stability, emphasizing the significance of picking a suitable oil phase

3343- QC,    Quercetin, a Flavonoid with Great Pharmacological Capacity
- Review, Var, NA - Review, AD, NA - Review, Arthritis, NA
*antiOx↑, Quercetin has a potent antioxidant capacity, being able to capture reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive chlorine species (ROC),which act as reducing agents by chelating transition-metal ions.
*ROS↓, Quercetin is a potent scavenger of reactive oxygen species (ROS), protecting the organism against oxidative stress
*angioG↓,
*Inflam↓, anti-inflammatory properties; the ability to protect low-density lipoprotein (LDL) oxidation, and the ability to inhibit angiogenesis;
*BioAv↓, It is known that the bioavailability of quercetin is usually relatively low (0.17–7 μg/mL), less than 10% of what is consumed, due to its poor water solubility (hydrophobicity), chemical stability, and absorption profile.
*Half-Life↑, their slow elimination since their half-life ranges from 11 to 48 h, which could favor their accumulation in plasma after repeated intakes
*GSH↑, Animal and cell studies have demonstrated that quercetin induces the synthesis of GSH
*SOD↑, increase in the expression of superoxide dismutase (SOD), catalase (CAT), and GSH with quercetin pretreatment
*Catalase↑,
*Nrf1↑, quercetin accomplishes this process involves increasing the activity of the nuclear factor erythroid 2-related factor 2 (NRF2), enhancing its binding to the ARE, reducing its degradation
*BP↓, quercetin has been shown to inhibit ACE activity, reducing blood pressure
*cardioP↑, quercetin has positive effects on cardiovascular diseases
*IL10↓, Under the influence of quercetin, the levels of interleukin 10 (IL-10), IL-1β, and TNF-α were reduced.
*TNF-α↓,
*Aβ↓, quercetin’s ability to modulate the enzyme activity in clearing amyloid-beta (Aβ) plaques, a hallmark of AD pathology.
*GSK‐3β↓, quercetin can inhibit the activity of glycogen synthase kinase 3β,
*tau↓, thus reducing tau aggregation and neurofibrillary tangles in the brain
*neuroP↑,
*Pain↓, quercetin reduces pain and inflammation associated with arthritis
*COX2↓, quercetin included the inhibition of oxidative stress, production of cytokines such as cyclooxygenase-2 (COX-2) and proteoglycan degradation, and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) (Nrf2/HO-1)
*NRF2↑,
*HO-1↑,
*IL1β↓, Mechanisms included decreased levels of TNF-α, IL-1β, IL-17, and monocyte chemoattractant protein-1 (MCP-1)
*IL17↓,
*MCP1↓,
PKCδ↓, studies with human leukemia 60 (HL-60) cells report that concentrations between 20 and 30 µM are sufficient to exert an inhibitory effect on cytosolic PKC activity and membrane tyrosine protein kinase (TPK) activity.
ERK↓, 50 µM resulted in the blockade of the extracellular signal-regulated kinases (ERK1/2) pathway
BAX↓, higher doses (75–100 µM) were used, as these doses reduced the expression of proapoptotic factors such as Bcl-2-associated X protein (Bax) and caspases 3 and 9
cMyc↓, induce apoptosis at concentrations of 80 µM and also causes a downregulation of cellular myelocytomatosis (c-myc) and Kirsten RAt sarcoma (K-ras) oncogenes
KRAS↓,
ROS↓, compound’s antioxidative effect changes entirely to a prooxidant effect at high concentrations, which induces selective cytotoxicity
selectivity↑, On the other hand, when noncancerous cells are exposed to quercetin, it exerts cytoprotective effects;
tumCV↓, decrease cell viability in human glioma cultures of the U-118 MG cell line as well as an increase in death by apoptosis and cell arrest at the G2 checkpoint of the cell cycle.
Apoptosis↑,
TumCCA↑,
eff↑, quercetin combined with doxorubicin can induce multinucleation of invasive tumor cells, downregulate P-glycoprotein (P-gp) expression, increase cell sensitivity to doxorubicin,
P-gp↓,
eff↑, resveratrol, quercetin, and catechin can effectively block the cell cycle and reduce cell proliferation in vivo
eff↑, cotreatment with epigallocatechin gallate (EGCG) inhibited catechol-O-methyltransferase (COMT) activity, decreasing COMT protein content and thereby arresting the cell cycle of PC-3 human prostate cancer cells
eff↑, synergistic treatment of tamoxifen and quercetin was also able to inhibit prostate tumor formation by regulating angiogenesis
eff↑, coadministration of 2.5 μM of EGCG, genistein, and quercetin suppressed the cell proliferation of a prostate cancer cell line (CWR22Rv1) by controlling androgen receptor and NAD (P)H: quinone oxidoreductase 1 (NQO1) expression
CycB/CCNB1↓, It can also downregulate cyclin B1 and cyclin-dependent kinase-1 (CDK-1),
CDK1↓,
CDK4↓, quercetin causes a decrease in cyclins D1/Cdk4 and E/Cdk2 and an increase in p21 in vascular smooth muscle cells
CDK2↓,
TOP2↓, quercetin is known to be a potent inhibitor of topoisomerase II (TopoII), a cell cycle-associated enzyme necessary for DNA replication
Cyt‑c↑, quercetin can induce apoptosis (cell death) through caspase-3 and caspase-9 activation, cytochrome c release, and poly ADP ribose polymerase (PARP) cleavage
cl‑PARP↑,
MMP↓, quercetin induces the loss of mitochondrial membrane potential, leading to the activation of the caspase cascade and cleavage of PARP.
HSP70/HSPA5↓, apoptotic effects of quercetin may result from the inhibition of HSP kinases, followed by the downregulation of HSP-70 and HSP-90 protein expression
HSP90↓,
MDM2↓, (MDM2), an onco-protein that promotes p53 destruction, can be inhibited by quercetin
RAS↓, quercetin can prevent Ras proteins from being expressed. In one study, quercetin was found to inhibit the expression of Harvey rat sarcoma (H-Ras), K-Ras, and neuroblastoma rat sarcoma (N-Ras) in human breast cancer cells,
eff↑, there was a substantial difference in EMT markers such as vimentin, N-cadherin, Snail, Slug, Twist, and E-cadherin protein expression in response to AuNPs-Qu-5, inhibiting the migration and invasion of MCF-7 and MDA-MB cells

5788- RES,    Calorie restriction-like effects of 30 days of Resveratrol (resVida™) supplementation on energy metabolism and metabolic profile in obese humans
- Trial, Nor, NA
*AMPK↑, In muscle, resveratrol activated AMPK, increased SIRT1 and PGC-1α protein levels,
*SIRT1↑, Resveratrol, which was discovered in a small-molecule screen as a potent SIRT1 activator
*PGC-1α↑,
*BP↓, Systolic blood pressure dropped and HOMA index improved after resveratrol.
*CRM↑, 30 days of resveratrol supplementation induces metabolic changes in obese humans, mimicking the effects of calorie restriction.
*Dose↝, resveratrol (150 mg/day (99%); resVida™)
*mtDam↓, Resveratrol increases AMPK activity, increases mitochondrial efficiency and respiration on fatty acid substrates.
*ALAT↓, paralleled by lower plasma ALAT values, as mentioned before, both indicating improved liver function.
*hepatoP↑,

2566- RES,    A comprehensive review on the neuroprotective potential of resveratrol in ischemic stroke
- Review, Stroke, NA
*neuroP↑, comprehensive overview of resveratrol's neuroprotective role in IS
*NRF2↑, Findings from previous studies suggest that Nrf2 activation can significantly reduce brain injury following IS and lead to better outcomes
*SIRT1↑, neuroprotective effects by activating nuclear factor erythroid 2-related factor 2 (NRF2) and sirtuin 1 (SIRT1) pathways.
*PGC-1α↑, IRT1 activation by resveratrol triggers the deacetylation and activation of downstream targets like peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) and forkhead box protein O (FOXO)
*FOXO↑,
*HO-1↑, ctivation of NRF2 through resveratrol enhances the expression of antioxidant enzymes, like heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1), which neutralize reactive oxygen species and mitigate oxidative stress in the ischemic bra
*NQO1↑,
*ROS↓,
*BP↓, Multiple studies have demonstrated that resveratrol presented protective effects in IS, it can mediate blood pressure and lipid profiles which are the main key factors in managing and preventing stroke
*BioAv↓, The residual quantity of resveratrol undergoes metabolism, with the maximum reported concentration of free resveratrol being 1.7–1.9 %
*Half-Life↝, The levels of resveratrol peak 60 min following ingestion. Another study found that within 6 h, there was a further rise in resveratrol levels. This increase can be attributed to intestinal recirculation of metabolites
*AMPK↑, Resveratrol also increases AMPK and inhibits GSK-3β (glycogen synthase kinase 3 beta) activity in astrocytes, which release energy, makes ATP available to neurons and reduces ROS
*GSK‐3β↓,
*eff↑, Furthermore, oligodendrocyte survival is boosted by resveratrol, which may help to preserve brain homeostasis following a stroke
*AntiAg↑, resveratrol may suppress platelet activation and aggregation caused by collagen, adenosine diphosphate, and thrombin
*BBB↓, Although resveratrol is a highly hydrophobic molecule, it is exceedingly difficult to penetrate a membrane like the BBB. However, an alternate administration is through the nasal cavity in the olfactory area, which results in a more pleasant route
*Inflam↓, Resveratrol's anti-inflammatory effects have been demonstrated in many studies
*MPO↓, Resveratrol dramatically lowered the amounts of cerebral infarcts, neuronal damage, MPO activity, and evans blue (EB) content in addition to neurological impairment scores.
*TLR4↓, TLR4, NF-κB p65, COX-2, MMP-9, TNF-α, and IL-1β all had greater levels of expression after cerebral ischemia, whereas resveratrol decreased these amounts
*NF-kB↓,
*p65↓,
*MMP9↓,
*TNF-α↓,
*IL1β↓,
*PPARγ↑, Previous studies have shown that resveratrol activates the PPAR -γ coactivator 1α (PGC-1 α), which has free radical scavenging properties
*MMP↑, Resveratrol can prevent mitochondrial membrane depolarization, preserve adenosine triphosphate (ATP) production, and inhibit the release of cytochrome c
*ATP↑,
*Cyt‑c∅,
*mt-lipid-P↓, mitochondrial lipid peroxidation (LPO), protein carbonyl, and intracellular hydrogen peroxide (H2O2) content were significantly reduced in the resveratrol treatment group, while the expression of HSP70 and metallothionein were restored
*H2O2↓,
*HSP70/HSPA5↝,
*Mets↝,
*eff↑, Shin et al. showed that 5 mg/kg intravenous (IV) resveratrol reduced infarction volume by 36 % in an MCAO mouse model.
*eff↑, This study indicates that resveratrol holds the potential to improve stroke outcomes before ischemia as a pre-treatment strategy
*motorD↑, resveratrol treatment significantly reduced infarct volume and prevented motor impairment, increased glutathione, and decreased MDA levels compared to the control group,
*MDA↓,
*NADH:NAD↑, Resveratrol treatment significantly enhanced the intracellular NAD+/NADH ratio
eff↑, Pretreatment with resveratrol (20 or 40 mg/kg) significantly lowered the cerebral edema, infarct volume, lipid peroxidation products, and inflammatory markers
eff↑, Intraperitoneal administration of resveratrol at a dose of 50 mg/kg reduced cerebral ischemia reperfusion damage, brain edema, and BBB malfunction

3967- Taur,    The Effects of Oral Taurine on Resting Blood Pressure in Humans: a Meta-Analysis
- Review, Nor, NA
*BP↓, These results translated to mean ~ 3 mmHg reductions in both SBP (range = 0-15 mmHg) and DBP (range = 0-7 mmHg) following a range of doses (1 to 6 g/day)

3951- Taur,    Taurine Supplementation Alleviates Blood Pressure via Gut–Brain Communication in Spontaneously Hypertensive Rats
- in-vivo, NA, NA
*BP↓, Taurine supplementation not only reduced the blood pressure, sympathetic activity, and inflammatory and oxidative stress in the PVN but also improved the cardiac pathology and microbiota composition while alleviating gut inflammation in hypertensive
*Inflam↓,
*ROS↓, Furthermore, the taurine treatment suppressed inflammation and the overproduction of ROS in the PVN in SHRs.
*cardioP↑,
*GutMicro↑, Taurine supplementation restored the microbiota balance, strengthened the mucosal barrier, reduced intestinal inflammation, and stimulated tryptophan metabolism.
*BBB↑, Moreover, the metabolites derived from the gut microbiota traverse the blood–brain barrier to reach the paraventricular nucleus, thereby reducing the inflammatory responses and oxidative stress, leading to decreased blood pressure in hypertensive rat

5904- TV,    Pharmacological Properties and Molecular Mechanisms of Thymol: Prospects for Its Therapeutic Potential and Pharmaceutical Development
- Review, Var, NA - Review, Stroke, NA - Review, Diabetic, NA - Review, Obesity, NA - Review, AD, NA - Review, Arthritis, NA
*antiOx↑, shown to possess various pharmacological properties including antioxidant, free radical scavenging, anti-inflammatory, analgesic, antispasmodic, antibacterial, antifungal, antiseptic and antitumor activities.
*ROS↓,
*Inflam↓,
*Bacteria↓,
AntiTum↑,
IronCh↑, chelation of metal ions
*HDL↑, antihyperlipidemic (via increasing the levels of high density lipoprotein cholesterol and decreasing the levels of low density lipoprotein cholesterol
*LDL↓,
*BioAv↝, videnced the presence of thymol in the stomach, intestine, and urine after its oral administration with sesame oil at a dose around 500 mg in rats and 1–3 g in rabbits.
*Half-Life↝, Oral administration of a single dose of thymol (50 mg/kg) was rapidly absorbed and slowly eliminated approximately within 24 h.The maximum concentration (Tmax) was reached after 30 min, while approximately 0.3 h was needed for the half-life
*BioAv↑, The rapid absorption of thymol indicates that it’s mainly absorbed in the upper component of the gut
*SOD↑, scavenging of free radicals by increasing the activities of several endogenous antioxidant enzymes levels viz. superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST)
*GPx↑,
*GSTs↑,
*eff↑, Thymol (0.02–0.20%) showed better antioxidant capacity than its isomer carvacrol in lipid systems due to its greater steric hindrance
radioP↑, Owing to its potent antioxidant potential, thymol showed radioprotective and anticlastogenic potential in gamma radiation induced Swiss albino mice
*MDA↓, Thymol supplementation increased the antioxidant status and decreased malondialdehyde (MDA) levels in broiler chickens
*other↑, Dietary supplementation with the combination of carvacrol–thymol (1:1) (100 mg/kg) reduced the occurrence of oxidative stress and the impairment of the intestinal barrier in weaning piglets by its potent antioxidant property
*COX1↓, by inhibiting both isoforms of cyclooxygenase (COX), with the most active being against COX-1 with an IC50 value of 0.2 μM.
*COX2↓,
*AntiAg↑, Thymol (1.1 μg/ml) exhibited inhibitory effects against arachidonic-acid-induced blood coagulation and platelet aggregation in vitro
*RNS↓, Thymol inhibited ROS (IC50= 3 μg/ml), reactive nitrogen species (RNS) (IC50= 4.7) and significantly reduced generation of NO and H2O2 as well as activities of nitric oxide synthase (NOS) and nicotinamide adenine dinucleotide reduced oxidase (NADH oxi
*NO↓,
*H2O2↓,
*NOS2↓,
*NADH↓,
*Imm↑, Thymol (25–200 mg/kg) was shown to modulate the immune system in cyclosporine-A treated Swiss albino mice by enhancing the expressions of cluster of differentiation 4 (CD4),
Apoptosis↑, anticancer actions of thymol include induction of apoptosis, anti-proliferation, inhibition of angiogenesis and migration
TumCP↓,
angioG↓,
TumCMig↓,
Ca+2↑, Intracellular Ca2+ overload
TumCCA↑, Cytotoxicity by stimulating cell cycle arrest in G0/G1 phase
DNAdam↑, DNA fragmentation, Bax protein expression, activation of caspase -9, -8 and -3 & concomitant PARP cleavage, AIF translocation
BAX↑,
Casp9↑,
Casp8↑,
Casp3↑,
cl‑PARP↑,
AIF↑,
i-ROS↑, intracellular ROS, depolarizing MMP, cytochrome-c release, cleavage of caspases, DNA fragmentation, activation of apaf-1,
MMP↓,
Cyt‑c↑,
APAF1↑,
Ca+2↑, In human glioblastoma cells, thymol (200–600 μM) produced a rise in (Ca2+)i levels
MMP9↓, diminished matrix metallopeptidase-9 (MMP9) and matrix metallopeptidase-2 (MMP2) production as well as protein kinase Cα (PKCα) and extracellular signal-regulated kinases (ERK1/2) phosphorylation
MMP2↓,
PKCδ↓,
ERK↓,
H2O2↑, Thymol increased the production of ROS and mitochondrial H2O2 thereby depolarizing mitochondrial membrane potential.
BAX↑, up-regulating Bcl-2 associated X protein (Bax) expression and down-regulating B-cell lymphoma (Bcl-2)
Bcl-2↓,
DNAdam↑, Thymol (IC50= 497 and 266 mM) was shown to induce DNA damage by increasing the levels of lipid peroxidation products;
lipid-P↑,
ChemoSen↑, This study recommended the combination of thymol with various chemotherapeutic agents to minimize its toxicity on normal cells and to improve the effectiveness of cancer treatment
chemoP↑,
*cardioP↑, significant increase in the activities of heart mitochondrial antioxidants (SOD, catalase, GPx, GSH)
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*BP↓, Thymol (1, 3, and 10 mg/kg) administration decreased the blood pressure and heart rate of Wistar rats whereas thymol (5 mg/kg) attenuated blood pressure in rabbits
*AntiDiabetic↑, protective effects of thymol in metabolic disorders such as diabetes mellitus and obesity
*Obesity↓,
RenoP↑, Thymol (20 mg/kg) was shown to inhibit cisplatin-induced renal injury by attenuating oxidative stress, inflammation and apoptosis in male adult Swiss Albino rats
*GastroP↑, This gastroprotective effect of thymol is believed to be due to increased mucus secretion
hepatoP↑, Thymol (150 mg/kg) showed to inhibit paracetamol induced hepatotoxicity in mice by preventing the alterations in the activities of hepatic marker enzymes
*AChE↓, Thymol (EC50= 0.74 mg/mL) was shown to possess acetylcholine esterase inhibitory activity but much less than its isomer carvacrol
*cognitive↑, Thymol (0.5–2 mg/kg) has been shown to inhibit cognitive impairments caused by increased Aβ levels or cholinergic hypofunction in Aβ
*BChE↓, whereas thymol (100 and 1000 μg/ml) also inhibited both AChE and butyrylcholinesterase (BChE) in a dose dependent manner
*other↓, Thymol (100 mg/kg) was shown to inhibit collagen induced arthritis by decreasing lipid peroxidation mediated oxidative stress by increasing the status of antioxidants in male Wistar rats
*BioAv↑, The encapsulation of thymol into methylcellulose microspheres by spray drying remarkably increases the bioavailability compared to free thymol


Showing Research Papers: 1 to 40 of 40

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 40

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   CYP1A1↓, 1,   GSH↓, 2,   H2O2↑, 1,   HO-1↑, 1,   lipid-P↑, 1,   NRF2↑, 2,   RNS↓, 1,   RNS↑, 1,   ROS↓, 3,   ROS↑, 6,   i-ROS↑, 1,   SOD2↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   mitResp↓, 1,   MMP↓, 2,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cMyc↓, 2,   CRM↑, 1,   Glycolysis↓, 1,   LDL↓, 2,   NADPH↓, 1,  

Cell Death ⓘ

Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 5,   Bak↑, 1,   BAX↓, 1,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Casp12↑, 1,   Casp3↑, 4,   Casp8↑, 2,   Casp9↑, 3,   Cyt‑c↑, 3,   Fas↑, 1,   MDM2↓, 1,   p38↑, 1,   Telomerase↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   HSP70/HSPA5↓, 1,   HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↑, 2,   P53↑, 1,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 3,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 2,   CDK4↓, 1,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

EMT↝, 1,   ERK↓, 2,   p‑GSK‐3β↓, 1,   HDAC1↓, 1,   IGF-1↓, 1,   mTOR↓, 1,   PI3K↓, 1,   PTEN↑, 1,   RAS↓, 1,   STAT3↓, 1,   TOP2↓, 1,   TumCG↓, 4,  

Migration ⓘ

Ca+2↑, 2,   E-cadherin↑, 1,   p‑FAK↓, 1,   KRAS↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   N-cadherin↓, 1,   PKCδ↓, 2,   TIMP2↑, 1,   TumCI↓, 1,   TumCMig↓, 3,   TumCP↓, 2,   TumCP↑, 1,   TumMeta↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 3,   VEGF↓, 2,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL8↓, 1,   Imm↑, 1,   Inflam↓, 1,   NK cell↑, 1,   PGE2↓, 1,  

Cellular Microenvironment ⓘ

pH↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   ChemoSen↑, 4,   eff↓, 1,   eff↑, 10,   eff∅, 1,   MDR1↓, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,   BP↓, 4,   KRAS↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 4,   AntiTum↑, 2,   cardioP↑, 1,   chemoP↑, 3,   chemoPv↑, 1,   ChemoSideEff↓, 1,   cognitive?, 1,   cognitive↑, 2,   hepatoP↑, 1,   memory↑, 1,   OS↑, 1,   QoL↑, 1,   radioP↑, 1,   RenoP↑, 1,   Risk↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 125

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 19,   ARE↑, 1,   Catalase↑, 10,   Ferroptosis↓, 1,   GPx↑, 6,   GSH↑, 7,   GSR↑, 1,   GSTs↑, 4,   H2O2↓, 2,   HDL↑, 3,   HO-1↑, 7,   Keap1↓, 1,   lipid-P↓, 8,   mt-lipid-P↓, 1,   MDA↓, 5,   Mets↝, 1,   MPO↓, 2,   NADH↓, 1,   NOX4↓, 1,   NQO1↑, 1,   Nrf1↑, 1,   NRF2↑, 9,   RNS↓, 1,   ROS↓, 23,   SOD↑, 11,   TAC↑, 1,   TBARS↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   Insulin↓, 1,   Insulin↑, 2,   MMP↑, 1,   mtDam↓, 1,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis ⓘ

adiP↑, 1,   ALAT↓, 2,   AMPK↑, 4,   cAMP↑, 1,   CRM↑, 2,   CYP3A2↓, 1,   glucose↓, 3,   H2S↑, 2,   HMG-CoA↓, 1,   LDH↓, 3,   LDL↓, 6,   NADH:NAD↑, 1,   NADPH↓, 1,   PPARα↝, 1,   PPARγ↑, 1,   SIRT1↑, 3,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↓, 1,   Casp↓, 1,   Casp6↓, 1,   Casp9↓, 1,   Cyt‑c∅, 1,   Fas↓, 1,   Ferroptosis↓, 1,   iNOS↓, 4,   JNK↓, 4,   MAPK↓, 1,   TRPV1↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↓, 3,   other↑, 8,   other↝, 3,   other∅, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   HSP70/HSPA5↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   ERK↑, 1,   FOXO↑, 1,   GSK‐3β↓, 2,   IGF-1↑, 1,   IGFBP1↑, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration ⓘ

5LO↓, 3,   AntiAg↑, 10,   AP-1↓, 2,   APP↓, 1,   Ca+2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   PKCδ↓, 1,   TRPC1↓, 1,   VCAM-1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   NO↓, 4,   TXA2↓, 1,  

Barriers & Transport ⓘ

BBB↓, 1,   BBB↑, 4,   GastroP↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 2,   COX2↓, 8,   CRP↓, 1,   ICAM-1↓, 2,   IFN-γ↑, 1,   IL1↓, 1,   IL10↓, 1,   IL17↓, 1,   IL1β↓, 6,   IL6↓, 7,   IL8↓, 1,   IL8↑, 1,   Imm↑, 3,   Inflam↓, 20,   MCP1↓, 1,   NF-kB↓, 10,   p‑NF-kB↓, 1,   p65↓, 1,   PGE2↓, 2,   TLR2↓, 1,   TLR4↓, 4,   TLR4↑, 1,   TNF-α↓, 10,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 4,   BChE↓, 1,   ChAT↑, 1,   tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 4,   NLRP3↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 4,   BioAv↑, 16,   BioAv⇅, 1,   BioAv↝, 6,   BioEnh↑, 1,   Dose↓, 1,   Dose↝, 7,   eff↓, 2,   eff↑, 13,   eff↝, 1,   Half-Life↑, 3,   Half-Life↝, 3,  

Clinical Biomarkers ⓘ

ALAT↓, 2,   AST↓, 1,   BP↓, 36,   creat↓, 2,   CRP↓, 1,   GutMicro↑, 6,   IL6↓, 7,   LDH↓, 3,   NOS2↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 2,   AntiCan↑, 1,   AntiDiabetic↑, 7,   cardioP↑, 18,   chemoP↑, 1,   chemoPv↑, 1,   cognitive↑, 14,   hepatoP↑, 4,   memory↑, 9,   motorD↑, 1,   neuroP↑, 18,   Obesity↓, 3,   OS↑, 2,   Pain↓, 2,   QoL↑, 2,   RenoP↑, 2,   Risk↓, 3,   toxicity↓, 4,   toxicity∅, 1,   Weight↓, 4,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 2,  
Total Targets: 169

Scientific Paper Hit Count for: BP, Blood Pressure
5 Chocolate
4 Allicin (mainly Garlic)
4 Chlorogenic acid
3 Resveratrol
3 Lycopene
3 Quercetin
2 Pterostilbene
2 Taurine
1 Anthocyanins
1 Alpha-Lipoic-Acid
1 beta-glucans
1 Bacopa monnieri
1 Capsaicin
1 Choline
1 Coenzyme Q10
1 Selenium
1 Calorie Restriction Mimetics
1 Hydroxycinnamic-acid
1 Spermidine
1 Aspirin -acetylsalicylic acid
1 diet Short Term Fasting
1 hydrogen sulfide
1 Potassium
1 Propolis -bee glue
1 Piperine
1 Phosphatidylserine
1 Thymol-Thymus vulgaris
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#:592  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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