BP Cancer Research Results
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*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
*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
*Inflam↓, It has anti-inflammatory, rheumatological, ulcer inhibiting, anticholinergic, analgesic, antimicrobial, antistress, antidiabetes, anticancer, liver protection, anthelmintics, antioxidants, antifungal, and wound healing propertie
*AntiBio↑,
*AntiDiabetic↑,
*hepatoP↑,
*antiOx↑,
*AntiFungal↑,
*Wound Healing↑,
*other↑, Garlic has a higher concentration of sulfur compounds (allicin, diallyl disulfide, S-allylcysteine, and diallyl trisulfide), which are responsible for its therapeutic properties.
*BP↓, Garlic consumption lowers blood pressure, inhibits atherosclerosis, decreases serum cholesterol and triglycerides, suppresses platelet aggregation, and increases fibrinolytic activity, among other things
*LDL↓,
*AntiAg↑,
*cognitive↑, Garlic can also aid in preventing cognitive decline by shielding neurons from neurotoxicity and apoptosis, which helps to prevent ischemia, obsessive-compulsive disorder (OCD), and neuronal death while also boosting learning and memory retention
*memory↑,
Risk↑, People who consumed more garlic had a 54% decreased risk of pancreatic cancer than those who consumed fewer amounts of garlic
*COX1↓, Garlic supplements have been demonstrated to reduce cyclooxygenase activity and thromboxane A2 production, resulting in antiplatelet action
*TXA2↓,
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↓,
*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↑,
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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/PTGS2↓,
*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/KDR/Flk1↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,
*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/PTGS2↓, 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
*LDH↓, Trans-anethole reduced LDH activity and inflammatory cell counts, including macrophage, neutrophil, and lymphocyte counts. trans-anethole 125mg/kg restored the histopathological changes induced in mouse lungs by PPE and LPS.
*IL6↓, trans-anethole reduced the serum concentrations of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), as well as significantly reducing blood pressure during chronic inflammation.
*TNF-α↓,
*BP↓,
*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.
*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.
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*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,
*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.
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*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/PTGS2↓,
*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
*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.
*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
*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↑,
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*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/PTGS2↓, 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].
*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
*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
*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
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*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].
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*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
*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
*toxicity↓, It has been demonstrated that oral administration of saffron extract at doses from 0.1 to 5 g/kg was non-toxic in mice
*lipid-P↓, crocetin showed significant effects on coronary heart disease by inhibiting lipoprotein oxidation
*neuroP↑, on neurodegenerative diseases [33, 39-44], on retinal function recovery by increasing retinal blood flow [33, 45], on reducing blood pressure and maintaining kidney function
*BloodF↑,
*BP↓,
*RenoP↑,
*ATP↑, enhance oxygen diffusivity during shock and reperfusion that ultimately lead to increased ATP production
AntiCan↑, Saffron and its derivatives particularly crocetin have demonstrated significant anticancer activity in breast, lung, pancreatic and leukemic cells.
TumCP↓, Breast Cancer MCF-7, MDA-MB-231 ↓Proliferation
Apoptosis↑, ↑Apoptosis
lipid-P↓, Liver Cancer Wistar rat (AFB1) C3H1OT1/2 cells ↓Lipid perxidation
ROS↓, Liver Cancer Wistar rat (AFB1)
C3H1OT1/2 cells ↓Reactive oxygen species
GSTs↑, Lung Cancer Swiss albino mice (B[a]P) ↓ Lipid peroxidation, ↑GST, ↑catalases, ↑superoxide dismutase
Catalase↑,
SOD↑,
*BloodF↓, Although clinical studies indicate improvements in flow-mediated dilation, they report only modest reductions in blood pressure,
*BP↓,
*BP↓, Relative to the placebo group, 24-hour BP fell 5.8/3.3 (systolic/diastolic) mm Hg and daytime BP fell 3.5/2.0 mm Hg with DHA.
*eff↝, Purified DHA but not EPA reduced ambulatory BP and HR in mildly hyperlipidemic men
*BP↓, Reductions in diastolic BP were greater following DHA [-3.4 mmHg (-1.3,-5.6), P = 0.002] and OO [-2.2 mmHg (0.08,-4.3), P = 0.04] compared with EPA.
*Dose↝, Overall, available evidence from RCTs indicates that provision of EPA+DHA reduces systolic blood pressure, while provision of ≥2 grams reduces diastolic blood pressure.
*BP↓, The strongest effects of EPA+DHA were observed among untreated hypertensive subjects (systolic blood pressure = −4.51mm Hg, 95% CI = −6.12 to −2.83; diastolic blood pressure = −3.05mm Hg, 95% CI = −4.35 to −1.74),
*Risk↓, Higher consumption of chocolate, cheese, and fermented milks (including yogurt) was associated with lower all-cause and CVD mortality.
*cardioP↑, Fermented milk consumption also showed a protective association with cancer mortality.
*GutMicro↑, Due to their diverse composition and influence on the gut microbiota, fermented foods are often considered functional foods, which justifies the growing scientific and public health interest in their relationship with long-term health outcomes.
*OS↑, As it can be seen, higher fermented milk consumption levels were associated with lower risk of all-cause mortality as compared to the lowest consumption levels (pooled RR = 0.941, p < 0.001).
*BP↓, Fermented dairy products (fermented milk, cheese) Bioactive peptides, SCFA, minerals (Ca, P, K), vitamin K2, CLA, lactic acid bacteria ACE inhibition and blood pressure regulation,
*GutMicro↑, Improving the gut microbiome and reducing inflammation through dietary inputs like fermented foods may therefore be a path to improving human health status
*Inflam↓,
*BP↓, figure 2
*LDL↓,
*HDL↑,
*CRP↓,
*IL6↓,
*TNF-α↓,
*Obesity↓,
*AntiDiabetic↑,
*cardioP↑, fermented dairy consumption was associated with a decreased risk of general CVD compared with controls
*GutMicro↑, yogurt consumption also coincided with transient increases in Streptococcus thermophilus and Bifidobacterium animalis subsp. lactis in feces, microbes commonly found in yogurt cultures, suggesting a role for the gut microbiome in mediating effects [
*neuroP↑, Evidence also suggests a potential protective role of fermented foods against age-related neurologic diseases such as dementia and Alzheimer’s disease.
*cognitive↑, 30 participants with Alzheimer’s disease found that daily consumption of 200 mL milk fermented with L. acidophilus, Lacticaseibacillus casei, B. bifidum, and Limosilactobacillus fermentum (2 × 109 CFU/g each) for 12 wk improved mini-mental state exam
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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
*cardioP↑, describes the cardioprotective potential of dandelion products and preparations.
*Dose↝, Dandelion is a rich source of phenolic acids (chicoric acid, chlorogenic acid), flavonoids (luteolin derivatives, quercetin), and terpenes (sesquiterpene lactones).
*Dose↝, It is also a strong source of vitamins (A, C, E, K, and B) and minerals (calcium, sodium, magnesium, iron, copper, silicon, zinc, manganese)
*toxicity∅, Although dandelion is mainly known for its medicinal properties, it has for many years been successfully used worldwide in the food industry as an entirely non-toxic and edible plant
*toxicity↓, dose should not exceed 4 g or 12 g per day for the aerial parts of the plant or 1 g or 3 g per day for the root. The roots, leaves, and flowers may be eaten raw or cooked
*BP↓, Dandelion leaves are also believed to have a positive effect on the cardiovascular system due to their high potassium content (397 mg potassium/100 g): increased potassium intake with food (about 3500 mg/day for an adult) has been found to lower BP
*Inflam↓, sesquiterpene lactones, which have been found to have anti-inflammatory and antibacterial effects, as well as triterpenes or phytosterols, which possess anti-atherosclerotic properties
*Bacteria↓,
*Imm↑, roots are also rich in inulin, which has a probiotic, hypoglycemic, and immune-boosting effect
*lipid-P↓, extract was found to elevate total antioxidant capacity and decrease lipid peroxidation, a marker of oxidative stress, in the heart, liver, kidney, and brain, among others.
*AST↓, ; treatment was found to improve the lipid profile and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) concentrations in obese mice.
*ALAT↓,
*AntiAg↑, extracts E2 and E3 and fractions A, B, and C significantly inhibited ADP-activated platelet adhesion to fibrinogen, while flavonoid fractions A to C inhibited thrombin-activated platelet adhesion at both tested doses (10 and 50 μg/mL)
*ROS↓, (1) the inhibition of reactive oxygen species (ROS) production;
*AntiThr↑, antithrombotic effects.
*cognitive↑, Folic acid supplementation appears to improve cognitive function and reduce blood levels of Aβ-related biomarkers in MCI.
*Aβ↓,
*BP↓,
*SAM-e↓, decreased (P < 0.05), while S-adenosylmethionine (SAM), SAM/SAH ratio, and the expression of DNA methyltransferase mRNA were increased
*DNMT3A↑,
*BP↓, After oral administration of ferulic acid (1 to 100 mg/kg) to SHR, systolic blood pressure (SBP) significantly decreased in a dose-dependent manner.
*Dose↝, When 7-week-old SHR were given 10 and 50 mg/kg/d of ferulic acid for 6 weeks, increases in BP were significantly attenuated compared to SHR on the control diet.
*memory↑, Significant improvements were observed on memory, while some of the studies also reported effects on attention and psychomotor speed or executive function.
*motorD↑,
*BP↓, Finally, studies reported improvements in blood pressure, but effects on metabolic risk markers (e.g. carbohydrate and lipid metabolism) were less consistent
*cognitive↑, beneficial effects of berry anthocyanins on cognitive performance as memory improved.
*antiOx↑, anti-oxidative, anti-inflammatory, anti-mutagenic and anti-carcinogenic properties coupled with their capacity to modulate key cellular enzyme function.
AntiCan↑,
*cardioP↑, Research on flavonoids received an added impulse with the discovery of the low cardiovascular mortality rate and also prevention of CHD.
*XO↓, They are also known to be potent inhibitors for several enzymes, such as xanthine oxidase (XO), cyclo-oxygenase (COX), lipoxygenase and phosphoinositide 3-kinase
*COX2/PTGS2↓,
*5LO↓,
*PI3K↓,
*AChE↓, A number of flavonoids have been reported for their anti-cholinesterase activity.
*Imm⇅, These effects indicate the immune-regulatory roles of flavonoids.
*BP↓, regular quercitin intake on blood pressure in overweight and obese patients with pre-hypertension and stage I hypertension was studied in seventy patients.
TumCCA↑, t pelingo juice induced cell accumulation in the G2/M phase of the cell cycle
*Aβ↓, certain flavonoids such as genistein, quercetin, taxifolin, kaemferol, luteolin, apigenin, daidzein, aminogeneistein, and α- and β-napthofalvone can affect Aβ production.
*BACE/β-secretase↓, direct inhibition of β active site cleavage enzyme-1 (BACE-1) activity
*NF-kB↓, inhibition of NF-κB activation by flavonoids
*ROS↓, flavones and catechins seem to be the most powerful flavonoids for protecting the body against reactive oxygen species.
*neuroP↑, like prevention of the neurodegeneration associated with AD and Parkinson's disease
*AntiAg↑, figure 3
*AntiThr↑,
*memory↑, Several reports have shown that GABA might affect brain protein synthesis, improve many brain functions such as memory and study capability, lower the blood pressure of spontaneously hypertensive rats, and may also have a relaxation effect in humans.
*BP↓,
*Dose↝, Capsules containing 100 mg of GABA or dextrin as a placebo were used as test samples.
*Stress↓, GABA might have alleviated the stress induced by the mental tasks
*toxicity↓, Data showed no serious adverse events associated with GABA at intakes up to 18 g/d for 4 days and in longer studies at intakes of 120 mg/d for 12 weeks.
*BP↓, GABA was associated with a transient and moderate drop in blood pressure (<10% change). intake of 80 mg/day of GABA was associated with a significant reduction of the BP in adults with mild hypertension, and no adverse effects were reported.
*AntiDiabetic↑, other biological activities, which include anti-hypertension, anti-diabetes, anti-cancer, antioxidant, anti-inflammation, anti-microbial, and anti-allergy effects
*AntiCan↑,
*antiOx↑,
*Inflam↓,
*AntiBio↑,
*other↝, GABA is a popular ingredient in sports dietary supplements and other wellness dietary supplements.
*cognitive↑, The NNHPD monograph for Cognitive Function Products recommends a daily intake of 50–3000 mg GABA that does not exceed 750 mg per single dose; it also says to consult a healthcare practitioner for use of products providing 300 mg/day or more when GABA
*GH↑, GABA has been reported to increase serum GH levels and has been considered an ergogenic aid. Many sports supplements include GABA as an ingredient.
*Sleep↑, insomnia improved more with 300 mg of GABA compared to 150 mg
*BioAv↑, GABA was rapidly absorbed (Tmax: 0.5~1 h)
*Half-Life↝, with a half-life of 5 h.
*BBB↓, very low amounts of GABA cross from the plasma into the brain through the BBB even when GABA is exogenously administered orally or intravenously
*eff↑, GABA and L-theanine had a synergistic effect on the sleep behavior of mice
*Dose↝, 20 mg as gamma-aminobutyric acid
*BP↓, Systolic blood pressure in the subjects given GABA-rich Chlorella significantly decreased compared with placebo
*eff↑, Reduction of SBP in the subjects with borderline hypertension was higher than those in the subjects with high-normal blood pressure.
*BBB↝, While traditional beliefs questioned GABA’s ability to cross the BBB, recent research challenges this notion, proposing specific transporter systems facilitating GABA passage.
*cognitive↑, literature suggests that oral intake of GABA affects the brain illustrated by changes in EEG scans and cognitive performance, with evidence showing that GABA can have beneficial effects for multiple age groups and conditions.
*Dose↝, The gut microbiota is a source of GABA present in the gut, but oral GABA intake needs to be considered as well.
*toxicity↓, A study found that consistent administration of GABA to rats and dogs, even at doses up to 1 g/kg/day, did not exhibit any indications of toxicity
*Stress↓, Another study looked at GABA’s ability to affect brain wave patterns and reported increasing alpha and decreasing beta waves suggesting relaxation
*Inflam↓, The anti-inflammatory activity of GABA-enriched products derived from Lactobacillus fermented rice bran solution exhibited inhibitory effects on the expression of inflammatory enzymes, including inducible nitric oxide synthase and cyclooxygenase-2, a
*iNOS↓,
*COX2/PTGS2↓,
*IL6↓, and reduced the generation of pro-inflammatory cytokines like interleukin (IL)-6, IL-1β, tumor necrosis factor α, and monocyte chemoattractant protein-1
*IL1β↓,
*TNF-α↓,
*Sleep↑, GABA rice containing 26.4 mg of GABA three times daily resulted in the improvement of insomnia scores as assessed by the Kupperman Menopause Index.
*Pain↓, oral GABA supplementation or microbial-derived GABA, as a promising avenue for pain management.
*neuroP↑, potential neuroprotective properties of GABA have garnered significant interest
*eff↑, Specifically, glutamate supplementation was found to enhance memory performance by increasing acetylcholine (ACh) levels, distinguishing its effects from those of GABA
*Ach↑,
*AST↓, In support of the impact of dietary GABA on the CNS, FL50 significantly reduced AST and ALT levels induced by EtOH
*ALAT↓,
*BP↓, revealed a significant reduction in blood pressure within 2 to 4 weeks of FMG intake, and this reduction was sustained throughout the 12-week intervention period.
*other↝, Quantitative analysis of the gut microbiota composition revealed a positive correlation between the abundance of Bacteroides and GABA levels. Individuals with higher concentrations of Bacteroides exhibited elevated GABA levels in the fecal samples,
*neuroP↑, possible positive effects of GABA, called a postbiotic, on neuroprotection, improving sleep quality, alleviating depression and relieving pain, the various health benefits of GABA-enriched foods such as antidiabetic, antihypertension, and anti-inflam
*Sleep↑,
*Pain↓,
*Inflam↓,
*BP↓,
*cognitive↑, GABA impacts cognitive functions such as cognition, emotion, and memory and controls central nervous system activity.
*memory↑,
*eff↑, GABA primarily exerts its influence through the brain–gut axis
*AChE↓, Research indicates that GABA derived from plant proteins such as beans, soybeans, and lentils exhibits high ACE inhibitor activity
*Wound Healing↑, GABA improved the reduction of overall healing duration and promoted early wound healing
*BP↓, Overall analyses found significant reductions for SBP (WMD = −6.077; 95% CI: −10.736 to −1.419; P = 0.011) and DBP (WMD = −2.803; 95% CI: −4.417 to −1.189; P = 0.001) after grape seed extract treatment
*eff↑, impact was more obvious in younger or obese subjects, as well as in patients with metabolic disorders.
*ROS↓, Overwhelming evidence from in vitro experiments suggests that grape seed extract has an antioxidant property that can protect cells from ROS-mediated DNA damage
*DNAdam↓,
*cardioP↑, French paradox that refers to the low rate of coronary heart disease mortality in France people despite the diets being rich in saturated fat.
*eff↝, With aging, it has been postulated that the effectiveness of grape seed extract on blood pressure regulation may be less obvious in the presence of these triggers. This proposition was substantiated in our age-stratified analysis.
*BP↓, GSE supplementation significantly reduced DBP (WMD: -2.20 mmHg, 95% CI: -3.79 to -0.60, I2 = 88.8%) and HR (WMD: -1.25 bpm, 95% CI: -2.32 to -0.19, I2 = 59.5%) but had no significant effects on FMD (WMD: 1.02%, 95% CI: -0.62 to 2.66, I2 = 92.0%) and
*Dose↝, Subjects consumed a juice (167 kJ (40 kcal)) containing 0 mg (Placebo) or 300 mg/d GSE (150 mg) twice daily for 6 weeks
*BP↓, GSE significantly reduced systolic BP (SBP) by 5·6 % (P=0·012) and diastolic BP (DBP) by 4·7 % (P=0·049) after 6 weeks of intervention period
*other↝, BP returned to baseline after the 4-week discontinuation period of GSE beverage
*eff↑, Subjects with higher initial BP experienced greater BP reduction; nearly double the effect size.
*Dose↝, Enovita (GSEe), a highly standardized extract in polyphenols of Vitis vinifera L. (300 mg/day for 16 weeks) Two GSEe tablets (150 mg each) were taken every day orally with sufficient water (one 5–10 min before breakfast and one 5–10 min before lunch)
*BP↓, GSEe resulted in a benefit of modulating endothelial functionality and blood pressure. It was noteworthy that GSEe relieved the perceived stress, promising new future perspectives on mood comfort.
*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,
*diuretic↑, The beverages of Hibiscus sabdariffa calyces are widely used in Mexico as diuretic, for treating gastrointestinal disorders, liver diseases, fever, hypercholesterolemia and hypertension
*BP↓, Different works have demonstrated that Hibiscus sabdariffa extracts reduce blood pressure in humans,
*ACE/ACE1↓, we demonstrated that this effect is due to angiotensin converting enzyme (ACE) inhibitor activity.
AntiCan↑, Hibiscus sabdariffa (HS) plant, including anthocyanin, flavonoids, saponins, tannins, polyphenols, organic acids, caffeic acids, citric acids, protocatechuic acid, and others, extracts of this plant have been reported to have anti-cancer effects.
TumCP↓, These compounds have been shown to reduce cancer cell proliferation, induce apoptosis, and cause cell cycle arrest.
Apoptosis↑,
TumCCA↑,
P53↑, They also increase the expression levels of the cell cycle inhibitors (p53, p21, and p27) and the pro-apoptotic proteins (BAD, Bax, caspase 3, caspase 7, caspase 8, and caspase 9).
P21↑,
p27/CDKN1B↑,
BAD↑,
BAX↑,
Casp3↑,
Casp7↑,
Casp8↑,
Casp9↑,
*AntiBio↑, Anti-microbial effect
*Inflam↓, Anti-inflammatory effect
*antiOx↑, In calyces of HS, compounds such as anthocyanins have antioxidant properties
*BP↓, The tea made from the HS leaves effectively lowers the blood pressure level in patients because of the presence of phytochemicals that induce systemic vasodilation along
*AntiDiabetic↑, calyces extract of HS can reduce the blood sugar level in diabetic patients
HDAC1↓, HS extract mediated inhibitory responses which were attributed to their inhibition of histone deacetylases (HDACs), specifically HDAC1 and HDAC3.
HDAC3↓,
tumCV↓, PCA dependently decreased cell viability, increased lactate dehydrogenase (LDH) leakage, enhanced DNA fragmentation, reduced mitochondrial membrane potential
LDL↓,
DNAdam↑,
MMP↓,
*Catalase↑, Ethanolic extract of the HS substantially increases the levels of the antioxidants CAT, SOD, GPx and reduced glutathione (GSH) in brain tissue, thus possessing significant antioxidant activity.
*SOD↑,
*GPx↑,
*GSH↑,
*antiOx↑,
*ROS↓, Anthocyanin in the extract of HS acts on the anti-oxidant system, and scavenges free radicals thus reducing damage to genomes of regular cells and the mutations, thus stopping tumor formation
TumCMig↓, PCA found in extract of HS inhibited cell migration and invasion to non-cytotoxic cells via down-regulation of the Ras/Akt/NF-κβ pathway and MMP-2 production [92].
TumCI↓,
selectivity↑,
RAS↓,
Akt↓,
NF-kB↓,
MMP2↓,
PI3K↓, decreasing PI3K, P-Akt protein, MMP expression, anti-apoptotic Bcl-2, Bcl-xL proteins, and PCNA, cyclin A, D1, B1, and E.
Bcl-2↓,
Bcl-xL↓,
PCNA↓,
cycA1/CCNA1↓,
cycD1/CCND1↓,
cycE/CCNE↓,
*BP↓, Data from 26 randomized controlled trials involving 1797 participants revealed that HS dose-dependently reduced systolic and diastolic BP compared to placebo and other teas.
*toxicity↓, Although HS is generally considered safe, long-term and therapeutic dosing safety requires careful monitoring.
*Dose↝, A dose escalation study ranging from 12 to 30 g/d of myo-inositol for a month was first conducted in 16 subjects
*toxicity↝, The maximum tolerated dose was found to be 18 g/d.
*BP↓, A statistically significant reduction in the systolic and diastolic blood pressures by an average of 10 mm Hg was observed after taking 18 g/d of myo-inositol for a month or more.
Showing Research Papers: 1 to 50 of 69
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 69
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↑, 1, CYP1A1↓, 1, GSH↓, 2, GSTs↑, 1, HO-1↑, 1, lipid-P↓, 1, NRF2↑, 2, RNS↓, 1, RNS↑, 1, ROS↓, 1, ROS↑, 4, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
mitResp↓, 1, MMP↓, 1, mtDam↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, cMyc↓, 1, CRM↑, 1, Glycolysis↓, 1, LDL↓, 2,
Cell Death(tgid=5) ⓘ
Akt↓, 2, Apoptosis↑, 4, BAD↑, 1, Bak↑, 1, BAX↑, 2, Bax:Bcl2↑, 1, Bcl-2↓, 3, Bcl-xL↓, 1, Casp12↑, 1, Casp3↑, 4, Casp7↑, 1, Casp8↑, 2, Casp9↑, 3, Cyt‑c↑, 1, Fas↑, 1, p27/CDKN1B↑, 1, p38↑, 1, Telomerase↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
CHK1↓, 1, DNAdam↑, 1, P53↑, 2, p‑P53↑, 1, PARP↑, 1, cl‑PARP↑, 1, PCNA↓, 2,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK2↓, 1, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 2, cycE/CCNE↓, 1, P21↑, 2, TumCCA↑, 5,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↝, 1, p‑GSK‐3β↓, 1, HDAC1↓, 1, HDAC3↓, 1, IGF-1↓, 1, mTOR↓, 1, PI3K↓, 2, RAS↓, 1, STAT3↓, 1, TumCG↓, 2,
Migration(tgid=13) ⓘ
E-cadherin↑, 1, p‑FAK↓, 1, MMP2↓, 1, N-cadherin↓, 1, TumCI↓, 1, TumCMig↓, 3, TumCP↓, 2, TumCP↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
Hif1a↓, 3, VEGF↓, 2, VEGFR2/KDR/Flk1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, IL8↓, 1, Imm↑, 1, Inflam↓, 1, NF-kB↓, 1, NK cell↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↝, 1, ChemoSen↑, 2, eff↓, 1, eff↑, 1, eff∅, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
BP↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 6, chemoP↑, 2, chemoPv↑, 1, ChemoSideEff↓, 1, cognitive?, 1, cognitive↑, 2, memory↑, 1, OS↑, 1, QoL↑, 1, Risk↓, 1, Risk↑, 1,
Infection & Microbiome(tgid=24) ⓘ
Bacteria↓, 1,
Total Targets: 101
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
ACE/ACE1↓, 1, AntiBio↑, 3, diuretic↑, 1, Stress↓, 2,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 17, Catalase↑, 5, Ferroptosis↓, 1, GPx↑, 3, GSH↑, 5, GSTs↑, 1, HDL↑, 3, HO-1↑, 2, Keap1↓, 1, lipid-P↓, 6, MDA↓, 2, MPO↓, 1, NRF2↑, 4, ROS↓, 17, SAM-e↓, 1, SOD↑, 5, TBARS↓, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, Insulin↓, 1, Insulin↑, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
adiP↑, 1, ALAT↓, 3, AMPK↑, 2, cAMP↑, 1, glucose↓, 3, H2S↑, 2, HMG-CoA↓, 1, LDH↓, 4, LDL↓, 6, NADPH↓, 1, PPARα↝, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Akt↑, 1, Apoptosis↓, 1, Casp↓, 1, Casp6↓, 1, Casp9↓, 1, Fas↓, 1, Ferroptosis↓, 1, iNOS↓, 3, JNK↓, 4, TRPV1↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 2, AntiThr↑, 2, other↓, 2, other↑, 3, other↝, 6, other∅, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1, DNMT3A↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↑, 1, GH↑, 1, IGF-1↑, 1, IGFBP1↑, 1, mTOR↓, 1, PI3K↓, 2,
Migration(tgid=13) ⓘ
5LO↓, 3, AntiAg↑, 11, APP↓, 1, Ca+2↓, 1, TRPC1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
Hif1a↓, 1, NO↓, 2, TXA2↓, 2,
Barriers & Transport(tgid=15) ⓘ
BBB↓, 1, BBB↑, 2, BBB↝, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX1↓, 1, COX2/PTGS2↓, 5, CRP↓, 1, IL1β↓, 2, IL6↓, 7, Imm↑, 3, Imm⇅, 1, Inflam↓, 18, NF-kB↓, 7, p‑NF-kB↓, 1, PGE2↓, 1, TLR4↓, 2, TNF-α↓, 8,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 4, ChAT↑, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 5, BACE/β-secretase↓, 1, NLRP3↓, 1, XO↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 4, BioAv⇅, 1, BioAv↝, 4, Dose↝, 15, eff↓, 2, eff↑, 11, eff↝, 3, Half-Life↝, 2,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 3, AST↓, 3, BloodF↓, 1, BloodF↑, 1, BP↓, 49, creat↓, 1, CRP↓, 1, GutMicro↑, 7, IL6↓, 7, LDH↓, 4,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 2, AntiCan↑, 2, AntiDiabetic↑, 10, cardioP↑, 17, chemoPv↑, 1, cognitive↑, 15, hepatoP↑, 3, memory↑, 11, motorD↑, 1, neuroP↑, 16, Obesity↓, 3, OS↑, 3, Pain↓, 3, QoL↑, 2, RenoP↑, 2, Risk↓, 4, Sleep↑, 3, toxicity↓, 9, toxicity↝, 1, toxicity∅, 1, Weight↓, 3, Wound Healing↑, 3,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, Bacteria↓, 2,
Total Targets: 137
Scientific Paper Hit Count for: BP, Blood Pressure
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
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