AntiAg Cancer Research Results

AntiAg, Antiplatelet aggregation: Click to Expand ⟱
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Antiplatelet aggregation refers to the process by which platelets clump together to form a blood clot.
The plethora of evidence indicates that among multiple hemostasis components, platelets play major roles in cancer progression by providing surface and granular contents for several interactions as well as behaving like immune cells.On the other hand, there are suggestions that antiplatelet treatment may promote solid tumor development in a phenomenon described as “cancers follow bleeding.” The controversies around antiplatelet agents justify insight into the subject to establish what, if any, role platelet-directed therapy has in the continuum of anticancer management.
The interplay between antiplatelet aggregation and cancer is an area of active research, with potential implications for therapeutic strategies. Antiplatelet agents, such as aspirin, are being investigated for their role in cancer prevention and treatment, particularly in reducing metastasis and improving patient outcomes.
Scientific Papers found: Click to Expand⟱
5345- ,    Effect of ajoene, the major antiplatelet compound from garlic, on platelet thrombus formation
- in-vitro, Nor, NA
*AntiAg↑, ajoene, the major antiplatelet compound from garlic

4574- AgNPs,    Advances in nano silver-based biomaterials and their biomedical applications
- Review, NA, NA
*Wound Healing↑, Antimicrobial effect of AgNPs allows effective use in wound healing and dentistry
*AntiThr↑, AgNPs possess antithrombotic activity useful to treat cardiovascular diseases.
*AntiAg↑, Their anti-platelet effects can be attributed to their ability to prevent or inhibit platelets from adhering to each other.
eff↑, AgNPs makes them excellent agents for photothermal therapy in the treatment of tumours and cancers.

4581- AgNPs,    Antimicrobial, anticoagulant and antiplatelet activities of green synthesized silver nanoparticles using Selaginella (Sanjeevini) plant extract
*Bacteria↓, SPE@Ag-NPs showed antibacterial, anticoagulant and antiplatelet activity.
*AntiAg↑,
*toxicity↓, SPE@Ag-NPs did not induce edema and hemorrhage in the experimental mice and also did not hydrolyze RBC cells suggesting its nontoxic property.

4580- AgNPs,    Biogenic Synthesis of Antibacterial, Hemocompatible, and Antiplatelets Lysozyme Functionalized Silver Nanoparticles through the One-Step Process for Therapeutic Applications
- in-vitro, NA, NA
*AntiAg↑, Platelet aggregation (0.19%) was not observed in the presence of 500 µL of 1 mM AgNPs (containing approx. 53.9 μg silver), suggesting the antiplatelet effect of AgNPs.

4579- AgNPs,    Response of platelets to silver nanoparticles designed with different surface functionalization
*AntiAg↑, Potentially, materials exhibiting antiplatelet activity may be applied in devices that prevent arterial thrombotic events like ischemic stroke, coronary heart disease, and ischemic gangrene.
*AntiThr↑,
*Dose↝, All four types of AgNPs were spherical in shape with the primary size close to 10 nm

4577- AgNPs,    Characterization of Antiplatelet Properties of Silver Nanoparticles
- vitro+vivo, Stroke, NA
*AntiAg↑, n the present study we show that nanosilver has an innate antiplatelet property and effectively prevents integrin-mediated platelet responses, both in vivo and in vitro, in a concentration-dependent manner
*Bacteria↓, We have recently reported synthesis of highly stable, uniformly sized silver nanoparticles endowed with enhanced antibacterial properties.
*Dose↝, Nanoparticles were spherical in shape, 10-15nm in diameter and monodispersed
*Dose↝, The extent of inhibition was the same irrespective of whether platelets were aspirinized or not. More than 80% (n $ 10) inhibition in amplitude was recorded at a nanoparticle concentration of 50 uM, which also reduced the slope of agregation/min
*Dose↝, (2!8 mg/kg body weight) in two different mice strains led to significant inhibition of platelet aggregation in mouse whole blood (studied by electronic impedance) in a dose-dependent manner
*toxicity↝, a dose of nanosilver up to 300 mg/kg was nontoxic to rodents.

4576- AgNPs,    Nanosilver, Next-Generation Antithrombotic Agent
- Study, NA, NA
*AntiAg↑, Together with its inherent antiplatelet and antibacterial properties,
*Bacteria↓,

5353- AL,    Aged Garlic Extract May Be Safe for Patients on Warfarin Therapy
- Human, Nor, NA
*AntiAg↑, Garlic has been known to have antiplatelet properties.
*toxicity↓, The results suggest that AGE is relatively safe and poses no serious hemorrhagic risk for closely monitored patients on warfarin oral anticoagulation therapy.
*cardioP↑, ts positive effects may be beneficial to people with a high-risk background or who are taking cardiovascular medications
*Dose↝, formulated by soaking sliced raw garlic in aqueous ethanol solution for up to 20 mo at room temperature. The extract was filtered and concentrated under reduced pressure at low temperature

2559- AL,    Effect of the Garlic Pill in comparison with Plavix on Platelet Aggregation and Bleeding Time
- Human, Nor, NA
AntiAg↑, Several studies indicated that garlic can inhibit platelet aggregation
COX2↓, garlic prevents inhibition of platelet aggregation by inhibiting cyclooxygenase activity and thus thromboxane A2 (TXA2) and B2 (TXB2
cardioP↑, Garlic can play an effective role in preventing and treating cardiovascular diseases.

2560- AL,    Effect of garlic on platelet aggregation in humans: a study in healthy subjects and patients with coronary artery disease
- ex-vivo, Nor, NA
*AntiAg↑, Garlic and its components are known to possess antiplatelet activity
BioAv↝, Though garlic components leave the body quickly, a slow build-up of the active ingredients may take place.
Dose↝, Each capsule contained oil equivalent to I g of raw garlic. oil extract of garlic was encapsulated. 2 capsules of garlic three times a day (i.e. 6 capsules/day) for a period of 1 month.

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↑,

2463- AL,    Garlic as an antithrombotic and antiplatelet aggregation agent
- Review, Nor, NA
AntiAg↑, This review suggests that garlic and its preparations have a beneficial effect against thrombosis and have an antiplatelet aggregation property.
other↑, Garlic been shown to inhibit platelet aggregation, both in vivo and in vitro

2658- AL,    The Toxic Effect Ways of Allicin on Different Cell Lines
- Review, Var, NA
*antiOx↑, The significant functional act of garlic is its anticancer, antimicrobial, antioxidant, antidiabetic, antifibrinolytic, immune enhancing, antiplatelet collected effect and its possible act in prohibiting cardiovascular illnesses
*AntiAg↑,
*cardioP↑,
Ca+2↑, Sultan et al.[34] stated that allicin is cytotoxic to monocytic leukemia cells (THP-1 cells) and stimulates calcium-linked hemolysis and eryptosis in human red blood cells. Allicin advances calcium grades in cells, reasons to oxidative stress and al
ROS↑, Allicin advances calcium grades in cells, reasons to oxidative stress and also induces CK1a, caspase, p38, mitogen-activated protein kinase
Casp↑,
p38↑,
MAPK↑,
hepatoP↑, Wu et al.[42] clarified that allicin applies hepaprotective action counter to hepatic toxicity of cells
chemoP↑, Throughout with other garlic preparations, aged garlic extract (AGE) has been indicated to have hepatoprotective, immune, improving, anticancer, and chemoprotective actions.

2640- Api,    Apigenin: A Promising Molecule for Cancer Prevention
- Review, Var, NA
chemoPv↑, considerable potential for apigenin to be developed as a cancer chemopreventive agent.
ITGB4↓, apigenin inhibits hepatocyte growth factor-induced MDA-MB-231 cells invasiveness and metastasis by blocking Akt, ERK, and JNK phosphorylation and also inhibits clustering of β-4-integrin function at actin rich adhesive site
TumCI↓,
TumMeta↓,
Akt↓,
ERK↓,
p‑JNK↓,
*Inflam↓, The anti-inflammatory properties of apigenin are evident in studies that have shown suppression of LPS-induced cyclooxygenase-2 and nitric oxide synthase-2 activity and expression in mouse macrophages
*PKCδ↓, Apigenin has been reported to inhibit protein kinase C activity, mitogen activated protein kinase (MAPK), transformation of C3HI mouse embryonic fibroblasts and the downstream oncogenes in v-Ha-ras-transformed NIH3T3 cells (43, 44).
*MAPK↓,
EGFR↓, Apigenin treatment has been shown to decrease the levels of phosphorylated EGFR tyrosine kinase and of other MAPK and their nuclear substrate c-myc, which causes apoptosis in anaplastic thyroid cancer cells
CK2↓, apigenin has been shown to inhibit the expression of casein kinase (CK)-2 in both human prostate and breast cancer cells
TumCCA↑, apigenin induces a reversible G2/M and G0/G1 arrest by inhibiting p34 (cdc2) kinase activity, accompanied by increased p53 protein stability
CDK1↓, inhibiting p34 (cdc2) kinase activity
P53↓,
P21↑, Apigenin has also been shown to induce WAF1/p21 levels resulting in cell cycle arrest and apoptosis in androgen-responsive human prostate cancer
Bax:Bcl2↑, Apigenin treatment has been shown to alter the Bax/Bcl-2 ratio in favor of apoptosis, associated with release of cytochrome c and induction of Apaf-1, which leads to caspase activation and PARP-cleavage
Cyt‑c↑,
APAF1↑,
Casp↑,
cl‑PARP↑,
VEGF↓, xposure of endothelial cells to apigenin results in suppression of the expression of VEGF, an important factor in angiogenesis via degradation of HIF-1α protein
Hif1a↓,
IGF-1↓, oral administration of apigenin suppresses the levels of IGF-I in prostate tumor xenografts and increases levels of IGFBP-3, a binding protein that sequesters IGF-I in vascular circulation
IGFBP3↑,
E-cadherin↑, apigenin exposure to human prostate carcinoma DU145 cells caused increase in protein levels of E-cadherin and inhibited nuclear translocation of β-catenin and its retention to the cytoplasm
β-catenin/ZEB1↓,
HSPs↓, targets of apigenin include heat shock proteins (61), telomerase (68), fatty acid synthase (69), matrix metalloproteinases (70), and aryl hydrocarbon receptor activity (71) HER2/neu (72), casein kinase 2 alpha
Telomerase↓,
FASN↓,
MMPs↓,
HER2/EBBR2↓,
CK2↓,
eff↑, The combination of sulforaphane and apigenin resulted in a synergistic induction of UGT1A1
AntiAg↑, Apigenin inhibit platelet function through several mechanisms including blockade of TxA
eff↑, ex vivo anti-platelet effect of aspirin in the presence of apigenin, which encourages the idea of the combined use of aspirin and apigenin in patients in which aspirin fails to properly suppress the TxA
FAK↓, Apigenin inhibits expression of focal adhesion kinase (FAK), migration and invasion of human ovarian cancer A2780 cells.
ROS↑, Apigenin generates reactive oxygen species, causes loss of mitochondrial Bcl-2 expression, increases mitochondrial permeability, causes cytochrome C release, and induces cleavage of caspase 3, 7, 8, and 9 and the concomitant cleavage of the inhibitor
Bcl-2↓,
Cyt‑c↑,
cl‑Casp3↑,
cl‑Casp7↑,
cl‑Casp8↑,
cl‑Casp9↑,
cl‑IAP2↑,
AR↓, significant decrease in AR protein expression along with a decrease in intracellular and secreted forms of PSA. Apigenin treatment of LNCaP cells
PSA↓,
p‑pRB↓, apigenin inhibited hyperphosphorylation of the pRb protein
p‑GSK‐3β↓, Inhibition of p-Akt by apigenin resulted in decreased phosphorylation of GSK-3beta.
CDK4↓, both flavonoids exhibited cell growth inhibitory effects which were due to cell cycle arrest and downregulation of the expression of CDK4
ChemoSen↑, Combination therapy of gemcitabine and apigenin enhanced anti-tumor efficacy in pancreatic cancer cells (MiaPaca-2, AsPC-1)
Ca+2↑, apigenin in neuroblastoma SH-SY5Y cells resulted in increased apoptosis, which was associated with increases in intracellular free [Ca(2+)] and Bax:Bcl-2 ratio, mitochondrial release of cytochrome c and activation of caspase-9, calpain, caspase-3,12
cal2↑,

2461- ASA,    Aspirin and platelets: the antiplatelet action of aspirin and its role in thrombosis treatment and prophylaxis
- Review, NA, NA
AntiAg↑, The antithrombotic action of aspirin (acetylsalicylic acid) is due to inhibition of platelet function by acetylation of the platelet cyclooxygenase (COX)
COX1↓, Aspirin is an approximately 150- to 200-fold more potent inhibitor of the (constitutive) isoform of the platelet enzyme (COX-1) than the (inducible) isoform (COX-2)
eff↑, Aspirin is the "gold standard" antiplatelet agent for prevention of arterial thromboses.

5415- ASA,    The Anti-Metastatic Role of Aspirin in Cancer: A Systematic Review
- Review, Var, NA
TumMeta↓, The included studies demonstrated that aspirin suppresses metastatic dissemination across multiple cancer types through coordinated platelet-dependent and tumor-intrinsic mechanisms.
COX1↓, Aspirin consistently inhibited platelet aggregation and COX-1-dependent TXA2 production, disrupting platelet–tumor cell interactions, intravascular metastatic niche formation, and platelet-mediated immune suppression.
TXA2↓,
AntiAg↑, Beyond platelet effects, aspirin suppressed EMT, migration, and invasion through modulation of EMT transcriptional regulators and inflammatory signaling pathways.
EMT↓,
TumCMig↓,
TumCI↓,
AMPK↑, Additional mechanisms included activation of AMPK, inhibition of c-MYC signaling, regulation of redox-responsive pathways and impairment of anoikis resistance.
cMyc↓,
PGE2↓, Importantly, oral aspirin (20 mg/kg/day; human-equivalent ≈ 150 mg/day), administered before tumor cell injection, prevented platelet-induced metastatic enhancement and suppressed TXA2 and PGE2 production.
Dose↑, medium and high doses of aspirin reduced pulmonary metastatic burden by more than 50%, whereas low-dose aspirin was ineffective.
RadioS↑, Wang et al. [45] demonstrated that low-dose aspirin suppresses radiotherapy-induced release of immunosuppressive exosomes in breast cancer, restoring NK-cell proliferation and enhancing antitumor immunity in vivo.
PD-L1↓, Similarly, Xiao et al. [46] showed that aspirin epigenetically downregulates PD-L1 expression by inhibiting KAT5-dependent histone acetylation, thereby restoring T-cell activation
E-cadherin↑, Aspirin restored E-cadherin expression and suppressed EMT regulators, including Slug, vimentin, Twist, MMP-2, and MMP-9.
EMT↓,
Slug↓,
Vim↓,
Twist↓,
MMP2↓,
MMP9↓,
other↑, definitive conclusions regarding clinical efficacy across cancer types cannot yet be drawn. Nevertheless, the consistency of mechanistic signals across experimental systems supports further investigation of aspirin as a low-cost adjunct in oncology

5412- ASA,    Clinical Pharmacology of Aspirin
- Review, NA, NA
*COX1↓, Aspirin is the acetate ester of salicylic acid and acts by binding irreversibly to cyclooxygenase-1 and cyclooxygenases-2
*COX2↓,
*cardioP↑, Aspirin is consumed most often at low-doses for cardio-protection and at higher doses as an analgesic, antipyretic, and anti-inflammatory agents.
*BioAv↑, Orally ingested aspirin is absorbed rapidly and the peak concentration is reached in about 1 hour.
*BioAv↝, a rise in pH also increases the solubility of aspirin and thus the dissolution of the tablets and the presence of food delays absorption of aspirin.
*Half-Life↓, The elimination half-life of aspirin in plasma is about 20 min
Risk↓, Patients who received 100 mg daily of aspirin had reduced risks of colorectal cancer and gastric cancer and an increased risk of gastrointestinal bleeding [6].
*other↑, Low-dose of aspirin treatment significantly improves ovarian responsiveness, uterine and ovarian blood flow velocity, and pregnancy-rates in women undergoing in-vitro fertilization [19].
*AntiAg↑, antiplatelet effect of aspirin [13],

5408- ASA,    An aspirin a day keeps cancer at bay
- Review, Var, NA
TumMeta↓, It has long been hypothesised that aspirin prevents cancer deaths by preventing metastasis.
TXA2↓, A recent study demonstrates this to be mediated through inhibition of Thromboxane A2 (TXA2) leading to reversal of suppression of T cell immunity.
*AntiAg↑, It was therefore hypothesised [3, 5] that aspirin prevents cancer metastasis, very likely through its anti-platelet action but the exact mechanism of action remained unclear.
COX1↓, anti-platelet activity through inhibition of cyclooxygenase-1 (COX-1) remains the main plausible mechanism.

5400- ASA,    Beyond COX-1: the effects of aspirin on platelet biology and potential mechanisms of chemoprevention
- Review, Nor, NA
Risk↓, dramatically reduced incidence of cancer in individuals taking daily low-dose aspirin [1–7],
*Inflam↓, Aspirin, like the vast majority of NSAIDs, is thought to exert its anti-inflammatory effects through inhibition of cyclooxygenase enzymes (COX enzymes) that regulate the production of prostaglandins.
*COX1↓,
*AntiAg↑, spirin acts to blunt a variety of pro-inflammatory responses, including the canonical inflammatory response [9–11], production of a defensive mucosal lining [12], and platelet aggregation [13, 14].
*Half-Life↓, The half-life of aspirin in the bloodstream was previously shown to be 13–19 min with a non-enzymatic hydrolysis rate of 0.023 min−1 at 37 °C in individuals given a single oral administration of aspirin.
*BioAv↑, Approximately 70% of aspirin reaches the peripheral circulation intact with maximum serum concentrations observed at 25 min after administration.

5401- ASA,    Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15R-prostaglandins that inhibit platelet aggregation
- Review, Nor, NA
*AntiAg↑, 15R-PGs are novel products of aspirin therapy via acetylation of COX-2 and may contribute to its antiplatelet and other pharmacologic effects.
*COX1↓, Aspirin inhibits the cyclooxygenase (COX) enzymes via a unique mechanism

5409- ASA,    Role of aspirin in cancer prevention
- Review, Var, NA
Imm↑, It was proved that aspirin showed advantages in immunomodulation, cell metabolism, gene repair, reduction of inflammatory reaction, anti-platelet activation and improvement of intestinal flora.
*Inflam↓,
*AntiAg↑, Clinicians have found that aspirin not only has anti-platelet aggregation, antipyretic, and analgesic effects, but also has a potential additional effect on the prevention and treatment of cancer.
*GutMicro↑,
eff↑, combination of aspirin and existing anti-tumor drugs also showed some synergistic effects.
TumMeta↓, The results showed that the aspirin group decreased the rate of distant metastasis, especially for colorectal cancer [3].
angioG↓, Studies have shown that aspirin can bind directly to the GLU150(Q9y251: Glu 225) region to inhibit heparanase activity and regulate related signalling pathways, thereby inhibiting angiogenesis and tumour metastasis [4].
Risk↓, A study published in the JAMA Network Open suggested that frequent aspirin use (defined as daily or almost daily use for 6 months or longer) was associated with a 13 % lower risk of ovarian cancer, and this protective association was not affected by
Risk↓, 1982 to 2009, and it was found that compared with non-aspirin users, men who take aspirin regularly (more than three tablets per week) have a lower risk of fatal prostate cancer.

4988- ATV,  Dipy,    Repurposing of the Cardiovascular Drug Statin for the Treatment of Cancers: Efficacy of Statin–Dipyridamole Combination Treatment in Melanoma Cell Lines
- in-vivo, Melanoma, NA
HMGCR↓, Metastatic melanoma has a very poor prognosis. Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR) inhibitors, are cholesterol-lowering agents with a potential for cancer treatment.
SREBP2↑, The inhibition of HMGCR by statins, however, induces feedback, which paradoxically upregulates HMGCR expression via sterol regulatory element-binding protein-2 (SREBP2)
SREBP2↓, Dipyridamole, an antiplatelet agent, is known to inhibit SREBP2 upregulation.
AntiAg↑,

4986- ATV,  Dipy,    The combination of statins and dipyridamole is effective preclinically in AML, MM, and breast cancer
- Review, Var, NA
HMG-CoA↓, Statins are drugs that have been utilized for years to treat hyperlipidemia through inhibition of the rate-limiting enzyme of the mevalonate (MVA) pathway, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR)
AntiAg↑, Dipyridamole (DP), a commonly prescribed anti-platelet agent potentiated the anti-cancer effects of atorvastatin
eff↑, DP-statin combination was synergistic and capable of inducing apoptosis in a variety of acute myelogenous leukemia (AML), MM and breast cancer cell lines.
Apoptosis↑, DP-statin combination also induced apoptosis in primary AML patient samples, but was not toxic to normal PBSCs.
selectivity↑,
*toxicity↓,
TumCG↓, In an in vivo AML tumor model, the DP-statin combination was found to be effective at inhibiting tumor growth.
PDE4↓, DP is known to elicit numerous effects, amongst them, phosphodiesterase (PDE) inhibition
other↑, . As both statins and DP are pre-approved for use in humans, off-patent, and readily available, they have the potential to directly impact patient care.

5366- AV,    Aloe vera: A review of toxicity and adverse clinical effects
- Review, Var, NA
*Dose↝, Chemical analysis reveals that the Aloe plant contains various polysaccharides and phenolic chemicals, notably anthraquinones.
*toxicity↝, lethal dose (LD50) in Swiss albino mice was 120.65 mg/kg.
tumCV↓, Aloe vera whole-leaf material caused a dose-dependent decrease in the viability in HeLa and HepG2 cells
*AntiAg↑, Aloe vera have antiplatelet effects,

4340- BBR,    Agonist-dependent differential effects of berberine in human platelet aggregation
- Human, NA, NA
*AntiAg↑, berberine selectively inhibits collagen-induced platelet aggregation
*other?, Since berberine was unable to inhibit the aggregation mediated by activation of thromboxane A2, increase in calcium influx, or stimulation of G-protein linked pathways, it is likely that berberine selectively inhibits platelet aggregation by interfer

4342- CA,    Antiplatelet effects of caffeic acid due to Ca(2＋) mobilizationinhibition via cAMP-dependent inositol-1, 4, 5-trisphosphate receptor phosphorylation
- in-vitro, NA, NA
*AntiAg↑, CAFA dose-dependently inhibited collagen-induced platelet aggregation and suppressed the production of TXA2, an aggregation-inducing autacoid associated with the strong inhibition of COX-1 in platelet microsomes exhibiting cytochrome C reductase acti
*TXA2↓, prevention of platelet aggregation-mediated thrombotic diseases.
*COX1↓,

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,

5825- CAP,    Bioavailability of capsaicin and its implications for drug delivery
- Review, Var, NA - Review, Arthritis, NA - Review, Obesity, NA
*AntiCan↑, Emerging studies show that it displays potent anti-tumor activity in several human cancers.
*TRPV1↑, The “heat-sensation” of capsaicin arises due to the binding of capsaicin to transient receptor potential vanilloid (TRPV) ion-channel receptors
*cardioP↑, some of the biological activities of capsaicin, like its anti-neoplastic, cardioprotective effects, have been found to be independent of the TRPV1 receptor.
AntiCan↓, Exposure to high doses of capsaicin (above 100 mg capsaicin per kg body weight) for a prolonged time causes peptic ulcers, accelerates the development of prostate, stomach, duodenal, and liver cancers and enhances breast cancer metastasis [5, 6].
Apoptosis↑, Capsaicin induces robust apoptosis in multiple types of human cancer cells both in vitro and in mice models.
ChemoSen↑, Capsaicin potentiates the apoptotic activity of cisplatin in human stomach cancer and attenuates cisplatin-induced renal toxicity in rodent models
*Inflam↓, oral or local administration of capsaicin reduces inflammation and pain from rheumatoid arthritis, fibromyalgia and chemical hyperalgesia
*Pain↓,
*AntiAg↑, The anti-platelet and anti-coagulant activity of capsaicin was independent of TRPV1
*Weight↓, capsaicinoids show anti-obesity activity by enhancing energy expenditure of the body
*BioAv↑, Capsaicin is robustly absorbed from the skin upon topical administration [4]
BioAv↑, capsaicin is rapidly absorbed from the stomach and the intestine following oral administration.
Half-Life↝, The liver and kidney displayed maximal amounts of capsaicin in 3 hours and 6 hours, respectively.
Half-Life↓, An interesting fact to note is that the bioavailability and half-life of capsaicin is quite low in the plasma, irrespective of the route of administration.

5881- CAR,    Carvacrol—A Natural Phenolic Compound with Antimicrobial Properties
- Review, Nor, NA
*Bacteria↓, Carvacrol, either alone or in combination with other compounds, has a strong antimicrobial effect on many different strains of bacteria and fungi that are dangerous to humans
*Inflam↓, Carvacrol also exerts strong anti-inflammatory properties by preventing the peroxidation of polyunsaturated fatty acids by inducing SOD, GPx, GR, and CAT, as well as reducing the level of pro-inflammatory cytokines in the body.
*SOD↑,
*GPx↑,
*GSR↑,
*Catalase↑,
*toxicity↓, Carvacrol is considered a safe compound despite the limited amount of data on its metabolism in humans.
*Pain↓, carvacrol has been used as a substitute for cretol and carbolic acid in the treatment of toothache, sensitive dentine, and alveolar abscess, and as an antiseptic in the pulp canals of the teeth
*other↑, because it has much greater activity as a mosquito repellent than the commercial preparation, N,N-diethyl-m-methylbenzamide
*cardioP↑, other biological activities, including cardio-, reno-, and neuroprotective [20]; immune response-modulating [21]; antioxidant; anti-inflammatory [22];
*RenoP↑,
*neuroP↑,
*antiOx↑,
*AntiDiabetic↑, antidiabetic; hepatoprotective [28]; and anti-obesity properties
*hepatoP↑,
*Obesity↓,
*AntiAg↑, figure 1
*BioAv↓, challenges surrounding the wider use of carvacrol in food or feed are its unpleasant and pungent taste at higher doses; low bioavailability;
BioAv↝, sensitivity to the surrounding environment, such as in processing conditions (e.g., heat or other ingredients); and the acidic environment in the digestive tract.
*OS↑, pneumonia. Administration of carvacrol to mice (10, 25, 50 mg/kg) was associated with increased survival and significantly reduced bacterial load
MMP↓, carvacrol was found to cause greater membrane depolarization and increased oxidative stress in E. coli cells;
ROS↑,
*MDA↓, In studies conducted in guinea pigs, carvacrol concentrations of 120 and 240 μg/mL have been shown to reduce malondialdehyde levels compared to the control group
*lipid-P↓, Carvacrol prevents lipid peroxidation by inducing SOD, GPx, GR, and CAT [85,86].
*COX2↓, A decrease in COX-2 gene expression was found at carvacrol concentrations of 0.008% and 0.016%
*Dose↝, Phase I clinical trial, carvacrol was administered to healthy subjects at 1 and 2 mg/kg/day for 1 month, and no critical adverse reactions

5888- CAR,    Therapeutic application of carvacrol: A comprehensive review
- Review, Var, NA - Review, Stroke, NA - Review, Diabetic, NA - Review, Park, NA
*antiOx↑, demonstrated as anti‐oxidant, anticancer, diabetes prevention, cardioprotective, anti‐obesity, hepatoprotective and reproductive role, antiaging, antimicrobial, and immunomodulatory properties.
*AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*Obesity↓,
*hepatoP↑,
*AntiAg↑,
*Bacteria↓,
*Imm↑,
MMP2↓, anticancer ability against malignant cells via decreasing the expressions of matrix metalloprotease 2 and 9, inducing apoptosis
MMP9↓,
Apoptosis↓,
MMP↓, disrupting mitochondrial membrane, suppressing extracellular signal‐regulated kinase 1/2 mitogen‐activated protein kinase signal transduction
ERK↓,
PI3K↓, decreasing the phosphoinositide 3‐kinase/protein kinase B.
ALAT↓, decreased the concentrations of alanine aminotransferase, alkaline phosphatase and aspartate aminotransferase,
*ROS↓, Essential oils found in plants are natural anti‐oxidants that reduce cell damage caused by reactive species and prevent mutagenic and carcinogenic processes.
*Catalase↑, Carvacrol has remarkably higher anti‐oxidative and hepatoprotective properties, which improves the activity of enzymatic anti‐oxidants (catalase, superoxide dismutase, and glutathione peroxidase)
*SOD↑,
*GPx↑,
*AST↓, Carvacrol decreased the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic acid dehydrogenase (LDH) and improved the status of inflammation, necrosis, and coagulation in the liver
*LDH↓,
*necrosis↓,
ROS↑, prostate cancer cells via lowering cell viability, increasing the rate of reactive oxygen species, and disrupting the mitochondrial membrane potential.
TumCCA↑, Carvacrol induced cell cycle arrest at G0/G1 that declined increased CDK inhibitor p21 expression and decreased cyclin‐dependent kinase 4 (CDK4), and cyclin D1 expressions.
CDK4↓,
cycD1/CCND1↓,
NOTCH↓, carvacrol inhibited Notch signaling in PC‐3 cells via downregulating Jagged‐1 and Notch‐1
IL6↓, human prostate cancer cell lines, which significantly reduced IL‐6
chemoP↑, Carvacrol has significant protective effects in reducing the side effects of chemotherapeutics such as irinotecan hydrochloride anticancer drugs that cause induction of intestinal mucositis.
*Pain↓, Pain management
*neuroP↑, The neuroprotective role of carvacrol was examined by Guan et al. in 2019 against ischemic stroke,
*TRPM7↓, downregulating TRPM7 channels
*motorD↑, improved catalepsy, akinesia, bradykinesia, locomotor activity, and motor coordination.
*NF-kB↓, Carvacrol reduced inflammatory biomarkers, such as nuclear factor κB and cyclooxygenase‐2, and levels of nitric oxides, malondialdehyde, and glutathione create oxidative stress.
*COX2↓,
*MDA↓,

5907- CAR,    Anti-proliferative and pro-apoptotic effect of carvacrol on human hepatocellular carcinoma cell line HepG-2
- in-vitro, Liver, HepG2
TumCG↓, In this study, we showed that carvacrol inhibited HepG2 cell growth by inducing apoptosis
Apoptosis↓,
Casp3↓, activation of caspase-3, cleavage of PARP and decreased Bcl-2 gene expression
cl‑PARP↑,
Bcl-2↓,
p‑ERK↓, decreasing phosphorylation of ERK1/2 significantly in a dose-dependent manner, and activated phosphorylation of p38
p‑p38↑,
*Bacteria↓, carvacrol has been shown to exhibit anti-microbial, anti-mutagenic, anti-platelet, analgesic, anti-inflammatory, anti-angiogenic, anti-oxidant, anti-elastase, insecticidal, anti-parasitic,cell-protective, AChE inhibitor and anti-tumor activity
*AntiAg↑,
*Inflam↓,
*antiOx↑,
*AChE↓,
AntiTum↑,
MMP↓, classical apoptosis response, including decrease in mitochondrial membrane potential and increase in cytochrome c release from mitochondria, decrease in Bcl-2/Bax ratio, increase in caspase activity and cleavage of PARP and fragmentation of DNA,
Cyt‑c↑,
Bax:Bcl2↑,
Casp↑,
DNAdam↑,
selectivity↑, we found that carvacrol induced stronger effects on hepatocellular carcinoma cells compared to normal human fetal liver cells.

5926- CAR,    An Updated Review of Research into Carvacrol and Its Biological Activities
- Review, Nor, NA - Review, AD, NA - Review, asthmatic, NA
*Inflam↓, ic, analgesic, anti-inflammatory,antioxidant, and neuroprotective effects.
*antiOx↑,
*neuroP↑, Carvacrol has exhibited notable neuroprotective effects in experimental models of cognitiveimpairment and neurodegenerative diseases
*BioAv↑, advances in encapsulation andnanotechnology have enhanced its stability and bioavailability
*toxicity↓, Compared to phenol, carvacrol and thymol exhibitsignificantly lower toxicity. This makes carvacrol a safer alternative for various applications, frombiological agents to dietary supplements [
*Pain↓, Pain-Relieving Mechanisms of Car
*TRPV3↑, , carvacrol-induced TRPV3 activation enhances lipolysis in adipocytes via theNRF2/FSP1 a
*NRF2↑,
*Ca+2↑, TRPV3 activation in distal colon epithelial cells elevates intracellular Ca²⁺ levels and stimulates ATP release, implicating carvacrol in gut physiology and signaling
*ATP↑,
*5LO↓, s, including the inhibition of angiotensin-converting enzyme 2 (ACE2), lipoxygenase(LOX), and cyclooxygenase (COX) enzyme
*COX2↓,
PGE2↓, arvacrol’s anti-inflammatory effects involve theinhibition of prostaglandin E₂ (PGE₂) production via COX-2
*hepatoP↑, Carvacrol in Hepatic Protection as Natural Antioxidant
*AntiAg↑, Carvacrol has demonstrated significant antiplatelet activity, highlighting its potential therapeutic role in preventing thrombosis
*Diar↓, s essentialoil exhibited antidiarrheal effects in castor oil-induced diarrhea models, potentially mediated bymechanisms involving Kv channel activation and Ca²⁺ channel inhibition
*cardioP↑, em as promising nutraceutical candidates for alleviatingCVD-related complicat
*other↝, Carvacrol was evaluated for its therapeutic potential in managing erectile dysfunction (ED)associated with aging
*chemoPv↑, Chemopreventive Potential of Carvacrol in Detoxification pathways
*cognitive↑, carvacrol(0.5–2 mg/kg) and thymol significantly improved cognitive function in rats
*AChE↓, potent acetylcholinesterase inhibitory activity (IC₅₀: 158.94 μg/mL)
*GastroP↑, . Gastroprotective Effects of Carvacrol and Mechanism
*eff↑, . When combined with polysorbate 80 as a surfactant, carvacrol was efficiently deliveredto embryonic tissues, maintaining bioavailability during the peri-hatching phase
*BChE↓, acrol. The essential oil rich in carvacrol showedstrong inhibitory effects on AChE and butyrylcholinesterase (BChE) [
*CRP↓, d Phase II clinical trial, asthmatic patients whoreceived 1.2 mg/kg/day of carvacrol for two months showed significant improvements in pulmonaryfunction tests and a notable reduction in C-reactive protein levek

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.

6011- CGA,    Chlorogenic Acid’s Role in Metabolic Health: Mechanisms and Therapeutic Potential
- Review, Nor, NA
*BioAv↓, CGA’s oral bioavailability remains limited, prompting research into optimized extraction methods, novel formulations, and structural modifications.
*antiOx↑, antioxidant, anti-inflammatory, anticancer, antibacterial, hepatoprotective, cardioprotective and neuroprotective effects, and modulation of lipid and glucose metabolism
*Inflam↓,
*Bacteria↓,
*hepatoP↑,
*cardioP↑,
*neuroP↑,
*ROS↓, CGA action include inhibition of oxidative stress, regulation of inflammatory responses through modulation of the NF-κB pathway and activation of the Nrf2 pathway
*NF-kB↓, inhibition of NF-κB
*NRF2↑,
*Obesity↓, Research demonstrates that CGA may influence body weight regulation through multiple pathways, including modulation of gut microbiota, reduction of inflammation, regulation of adipogenesis, and stimulation of thermogenesis.
*GutMicro↑, increasing the abundance of probiotic bacteria such as Bifidobacterium and Lactobacillus, while reducing the abundance of bacterial strains found in obese patients and animals, such as Desulfovibrionaceae, Ruminococcaceae, Lachnospiraceae, and Erysip
*AntiAg↑, antiplatelet effects of CGA are supported by both in vitro and in vivo studies
*cardioP↑, CGA was recognized as a compound with high cardioprotective potential, considering its antioxidant, anti-inflammatory, and antihypertensive activities
*AntiDiabetic↑, CGA alleviates the effects of type 2 diabetes mellitus (DM) and helps prevent its development
*NLRP3↓, CGA also inhibits the NLRP3 inflammasome via Nrf2 activation, significantly decreasing proteinuria, creatinine, and urea levels in diabetic rats
*OCLN↓, figure 3
*VEGF↓,
BioAv↝, CGA is water-soluble but highly unstable when exposed to elevated temperature, light, oxygen, or alkaline pH

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↑,

3890- Cin,    The Therapeutic Roles of Cinnamaldehyde against Cardiovascular Diseases
- Review, NA, NA
*cardioP↑, CA-related cardiovascular protective mechanisms could be attributed to the inhibition of inflammation and oxidative stress, improvement of lipid and glucose metabolism
*Inflam↓,
*ROS↓,
*lipid-P↓,
*AntiAg↑, suppression of cardiac fibrosis, and platelet aggregation and promotion of vasodilation and angiogenesis.
*angioG↑,
*GutMicro↑, CA is likely to inhibit CVD progression via affecting other possible processes including autophagy and ER stress regulation, gut microbiota and immune homeostasis, ion metabolism, ncRNA expression, and TRPA1 activation.
*ER Stress↓,

4337- CUR,    Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling
- in-vitro, NA, NA
*AntiAg↑, We show that curcumin inhibited platelet aggregation mediated by the platelet agonists epinephrine (200 μM), ADP (4 μM), platelet-activating factor (PAF; 800 nM), collagen (20 μg/mL), and arachidonic acid (AA: 0.75 mM).
*TXA2↓, results suggest that the curcumin-mediated preferential inhibition of PAF- and AA-induced platelet aggregation involves inhibitory effects on TXA2 synthesis and Ca2+ signaling, but without the involvement of PKC.

2466- CUR,    Regulatory Effects of Curcumin on Platelets: An Update and Future Directions
- Review, Nor, NA
*AntiAg↑, Several studies have proved the beneficial role of curcumin on platelets . in-vivo study exhibited that curcumin inhibited platelet aggregation in monkeys
*antiOx↑, Curcumin exhibits promising antioxidant activity
*Inflam↓,
*12LOX↑, increased the production of 12-LOX
COX1↓, Curcuminoids have been demonstrated to inhibit cyclo-oxygenase and 12-lipoxygenase activities in human platelets, thus showing antioxidant activity
COX2↓, Its effectiveness in cancer is mediated by inhibition of COX-2, MMP-9, and NF-kB
MMP9↓,
NF-kB↓,

4989- Dipy,    Dipyridamole
- Review, NA, NA
AntiAg↑, Dipyridamole is an antiplatelet agent commonly used for secondary stroke prevention and as an adjunct to warfarin therapy in patients with mechanical heart valves.

4341- EA,    Novel Bioactivity of Ellagic Acid in Inhibiting Human Platelet Activation
- in-vitro, NA, NA
*AntiAg↑, Ellagic acid (20 to 80 μ M) exhibited a potent activity in inhibiting platelet aggregation stimulated by collagen; however, it did not inhibit platelet aggregation stimulated by thrombin, arachidonic acid, or U46619.
*AntiAg↑, Treatment with ellagic acid (50 and 80 μ M) significantly inhibited platelet activation stimulated by collagen; this alteration was accompanied by the inhibition of relative [Ca(2+)] i mobilization, and the phosphorylation of phospholipase C (PLC) γ

2562- EGCG,    Green Tea Epigallocatechin 3-Gallate Reduced Platelet Aggregation and Improved Anticoagulant Proteins in Patients with Transfusion-Dependent β-Thalassemia: A Randomized Placebo-Controlled Clinical Trial
- Trial, NA, NA
AntiAg↑, in vitro treatment of GTE (at least 1 mg EGCG equivalent) inhibited PLT aggregation in patients who were healthy and with thalassemia platelet-rich plasma (PRP),
other↝, The results indicated that there were no significant differences in PT and aPTT values between the placebo group and the two groups receiving GTE tablets (50 and 100 mg EGCG equivalent) at the same time points during the intervention.

2563- EGCG,    Cardioprotective effect of epigallocatechin gallate in myocardial ischemia/reperfusion injury and myocardial infarction: a meta-analysis in preclinical animal studies
- Review, NA, NA
cardioP↑, EGCG significantly improves cardiac function, serum myocardial injury enzyme, and oxidative stress levels in MIRI animal models
ROS↑,
AntiAg↑, EGCG can inhibit platelet aggregation induced by U46619, collagen, arachidonic acid, and toxic carotenoids and shear force-induced platelet adhesion dose-dependently by suppressing PLCγ2 and tyrosine phosphorylation
eff↑, What’s more, its combination with common antiplatelet therapeutic agents, aspirin (ASA), clopidogrel (CPD), and tiglitazarol (TCG), did not further inhibit platelet aggregation resulting in bleeding complications
COX1↓, EGCG inhibits platelet activation by inhibiting microsomal cyclooxygenase-1 activity in platelets

2468- EGCG,    Green tea epigallocatechin-3-gallate inhibits platelet signalling pathways triggered by both proteolytic and non-proteolytic agonists
- in-vitro, Nor, NA
*AntiAg↑, EGCG inhibits platelet activation, by hindering the thrombin proteolytic activity, and by reducing the agonist-induced [Ca(2+)](c) increase through inhibition of Syk and Lyn activities.
*Ca+2↓,

2561- EGCG,  ASA,    Anti-platelet effects of epigallocatechin-3-gallate in addition to the concomitant aspirin, clopidogrel or ticagrelor treatment
- ex-vivo, Nor, NA
AntiAg↑, EGCG significantly reduced ADP- and COL-induced platelet aggregation in dose-dependent manner
eff↑, no further increase of bleeding risk by EGCG in the participants who were already taking other anti-platelet agents.
Half-Life↝, half-life of EGCG is approximately 3 hours
other∅, EGCG significantly inhibited the human platelet aggregation without any changes on P-selectin and PAC-1 expressions.

3722- Gb,    Alzheimer's disease: Research summaries – Do Ginkgo products help?
- Review, AD, NA
*memory↑, The studies showed that taking a higher dose of the Ginkgo extract (240 mg per day) could improve participants' memory.
*AntiAg↑, believed that it can increase the effect of blood-thinning medications such as acetylsalicylic acid (the drug in medications like Aspirin) and warfarin.

2464- GI,    The Effect of Ginger (Zingiber officinale) on Platelet Aggregation: A Systematic Literature Review
- Review, Nor, NA
*Inflam↓, gingerol and shogaol classes of compounds, might exert several beneficial effects including anti-inflammatory, antioxidant, and cholesterol lowering properties
*antiOx↑,
*LDL↓,
*AntiAg↑, previous clinical trials report few side-effects, mostly minor in nature (e.g. mild nausea, heartburn).[1] Of these reported side effects, potentially the most significant is an antiplatelet effect.
*AntiAg∅, In contrast, two studies reported that 2–3.6g of ginger had no effect on measures of platelet aggregation in health adults.

3770- H2,    Role of Molecular Hydrogen in Ageing and Ageing-Related Diseases
- Review, AD, NA - Review, Park, NA
*antiOx↑, antioxidative properties as it directly neutralizes hydroxyl radicals and reduces peroxynitrite level
*NRF2↑, activates Nrf2 and HO-1, which regulate many antioxidant enzymes and proteasomes.
*HO-1↑,
*Inflam↓, hydrogen may prevent inflammation
*neuroP↑, prevention and treatment of various ageing-related diseases, such as neurodegenerative disorders, cardiovascular disease, pulmonary disease, diabetes, and cancer.
*cardioP↑,
*other↓, It also prevented ischemia-reperfusion (I/R) injury and stroke in a rat model
*ROS↓, H2 has been shown to exert its beneficial effects in various pathological conditions that involve free radicals and oxidative stress
*NADPH↓, figure 2, H2 Inhibits NADPH Oxidase Activity
*Catalase↑,
*GPx1↑,
*NO↓, H2 Indirectly Reduces Nitric Oxide (NO) Production
*mt-ROS↓, H2 Decreases Mitochondrial ROS
*SIRT3↑, In the kidneys, H2 suppressed the downregulated Sirt3 expression, which is the most abundant member of the sirtuin family, by reducing oxidative stress reactions
*SIRT1↑, In the liver, H2 elevated HO-1 to induce Sirt1 expression
*TLR4↓, H2 inhibits TLR4, which involves hyperglycemia in type 2 diabetes mellitus
*mTOR↓, For example, H2 inhibits mTOR, activates autophagy, and alleviates cognitive impairment resulting from sepsis
*cognitive↑,
*Sepsis↓,
*PTEN↓, It inhibits the activation of the PTEN/AKT/mTOR pathway and alleviates peritoneal fibrosis
*Akt↓,
*NLRP3↓, It also facilitates autophagy-mediated NLRP3 inflammasome inactivation and alleviates mitochondrial dysfunction and organ damage
*AntiAg↑, antiageing mechanism of H2 and the influence on ageing hallmarks are summarized in Figure 3.
*IL6↓, significantly suppressed inflammatory cytokines (IL-6, TNF-α, and IL-1β), MDA, and 8-OHdG, and improved memory dysfunction
*TNF-α↓,
*IL1β↓,
*MDA↓,
*memory↑,
*FOXO3↑, HRW can also upregulate Sirt1-Forkhead box protein O3a (FOXO3a
TumCG↓, H2 inhibits lung cancer progression
*LDL↓, Decreases oxidized LDL; improves HDL function


Showing Research Papers: 1 to 50 of 82
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 82

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

CYP1A1↓, 1,   RNS↑, 1,   ROS↑, 6,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 3,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 2,   cMyc↓, 1,   FASN↓, 1,   HMG-CoA↓, 1,   SREBP2↓, 1,   SREBP2↑, 1,  

Cell Death ⓘ

Akt↓, 1,   APAF1↑, 1,   Apoptosis↓, 2,   Apoptosis↑, 3,   Bak↑, 1,   BAX↑, 1,   Bax:Bcl2↑, 2,   Bcl-2↓, 3,   Casp↑, 3,   Casp3↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   cl‑Casp7↑, 1,   cl‑Casp8↑, 1,   cl‑Casp9↑, 1,   CK2↓, 2,   Cyt‑c↑, 3,   cl‑IAP2↑, 1,   p‑JNK↓, 1,   MAPK↑, 1,   p38↑, 1,   p‑p38↑, 1,   Telomerase↓, 2,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 3,   other↝, 1,   other∅, 1,   p‑pRB↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   HSPs↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↓, 1,   cl‑PARP↑, 3,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK4↓, 2,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   ERK↓, 2,   p‑ERK↓, 1,   p‑GSK‐3β↓, 1,   HMGCR↓, 1,   IGF-1↓, 1,   IGFBP3↑, 1,   NOTCH↓, 1,   PI3K↓, 1,   TumCG↓, 3,  

Migration ⓘ

AntiAg↑, 11,   Ca+2↑, 2,   cal2↑, 1,   E-cadherin↑, 2,   FAK↓, 1,   ITGB4↓, 1,   MMP2↓, 2,   MMP9↓, 3,   MMPs↓, 1,   Slug↓, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↑, 1,   TumMeta↓, 4,   Twist↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   Hif1a↓, 2,   TXA2↓, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 5,   COX2↓, 3,   IL6↓, 1,   Imm↑, 1,   NF-kB↓, 1,   PD-L1↓, 1,   PGE2↓, 2,   PSA↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 4,   ChemoSen↑, 2,   Dose↑, 1,   Dose↝, 1,   eff↑, 9,   Half-Life↓, 1,   Half-Life↝, 2,   RadioS↑, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AR↓, 1,   EGFR↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 1,   PD-L1↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↓, 1,   AntiTum↑, 1,   cardioP↑, 2,   chemoP↑, 2,   chemoPv↑, 2,   cognitive↑, 1,   hepatoP↑, 1,   PDE4↓, 1,   Risk↓, 4,  
Total Targets: 117

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 13,   Catalase↑, 5,   Ferroptosis↓, 1,   GPx↑, 2,   GPx1↑, 1,   GSH↑, 1,   GSR↑, 1,   HDL↑, 1,   HO-1↑, 2,   lipid-P↓, 3,   MDA↓, 3,   NRF2↑, 4,   ROS↓, 8,   mt-ROS↓, 1,   SIRT3↑, 1,   SOD↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   Insulin↑, 2,  

Core Metabolism/Glycolysis ⓘ

12LOX↑, 1,   glucose↓, 1,   H2S↑, 1,   LDH↓, 1,   LDL↓, 3,   NADPH↓, 2,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Ferroptosis↓, 1,   JNK↓, 2,   MAPK↓, 1,   necrosis↓, 1,   TRPV1↑, 2,  

Kinase & Signal Transduction ⓘ

TRPV3↑, 1,  

Transcription & Epigenetics ⓘ

AntiThr↑, 2,   other?, 1,   other↓, 2,   other↑, 2,   other↝, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

FOXO3↑, 1,   mTOR↓, 1,   PTEN↓, 1,   TRPM7↓, 1,  

Migration ⓘ

5LO↓, 2,   AntiAg↑, 41,   AntiAg∅, 1,   Ca+2↓, 1,   Ca+2↑, 1,   PKCδ↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   NO↓, 1,   TXA2↓, 3,   VEGF↓, 1,  

Barriers & Transport ⓘ

GastroP↑, 1,   OCLN↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 4,   COX2↓, 4,   CRP↓, 1,   IL1β↓, 1,   IL6↓, 1,   Imm↑, 2,   Inflam↓, 15,   NF-kB↓, 5,   TLR4↓, 2,   TNF-α↓, 1,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   BChE↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 6,   BioAv⇅, 1,   BioAv↝, 3,   Dose↝, 8,   eff↓, 1,   eff↑, 1,   Half-Life↓, 2,  

Clinical Biomarkers ⓘ

AST↓, 1,   BP↓, 7,   CRP↓, 1,   GutMicro↑, 4,   IL6↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 3,   AntiDiabetic↑, 4,   cardioP↑, 15,   chemoPv↑, 2,   cognitive↑, 4,   hepatoP↑, 4,   memory↑, 2,   motorD↑, 1,   neuroP↑, 6,   Obesity↓, 4,   OS↑, 1,   Pain↓, 5,   RenoP↑, 1,   Risk↓, 2,   toxicity↓, 6,   toxicity↝, 2,   Weight↓, 1,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 7,   Diar↓, 1,   Sepsis↓, 1,  
Total Targets: 103

Scientific Paper Hit Count for: AntiAg, Antiplatelet aggregation
8 Aspirin -acetylsalicylic acid
8 Resveratrol
7 Silver-NanoParticles
6 Allicin (mainly Garlic)
6 Hydrogen Gas
4 Carvacrol
4 Chocolate
4 EGCG (Epigallocatechin Gallate)
3 Dipyridamole
3 Lycopene
2 Atorvastatin
2 Capsaicin
2 Chlorogenic acid
2 Curcumin
2 Luteolin
2 Magnolol
2 Piperlongumine
2 Quercetin
2 Rutin
1 Apigenin (mainly Parsley)
1 Aloe anthraquinones
1 Berberine
1 Caffeic acid
1 Cinnamon
1 Ellagic acid
1 Ginkgo biloba
1 Ginger/6-Shogaol/Gingerol
1 Honokiol
1 Potassium
1 Naringin
1 Oleocanthal
1 Selenium NanoParticles
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#:10  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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