| Features: polyphenol | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Found in red grapes and products made with grapes. Resveratrol is a polyphenol compound found in various plant species, including grapes, berries, and peanuts. • Anti-inflammatory effects, Antioxidant effects: - Antiplatelet aggregation for stroke prevention - BioAvialability use piperine - some sources may use Japanese knotweed roots (Reynoutria Japonica - root) as source which might contain Emodin (laxative) -known as Nrf2 activator, both in cancer and normal cells. Which raises controversity of use in ROS↑ therapies. Interestingly there are reports of NRF2↑ and ROS↑ in cancer cells. This raises the question of if it is a chemosensitizer. However other reports indicate NRF2 droping with Res, indicating it maybe a chemosenstizer. - RES is also considered to be them most effective natural SIRT1↑ -activating compound (STACs). However, in the presence of certain metals, such as copper or iron, resveratrol can undergo a process called Fenton reaction, which can lead to the generation of reactive oxygen species (ROS). The pro-oxidant effects of resveratrol are often observed at high concentrations, typically above 50-100 μM, and in the presence of certain metals or other pro-oxidant agents. In contrast, the antioxidant effects of resveratrol are typically observed at lower concentrations, typically below 10-20 μM. Clinical trials have used doses ranging from 150 mg to 5 grams per day. Lower doses (< 1 g/day) are often well-tolerated, but higher doses might be necessary for therapeutic effects and can be associated with side effects. -Note half-life 1-3 hrs?. BioAv poor: min 5uM/L required for chemopreventive effects, but 25mg Oral only yeilds 20nM. co-administration of piperine Pathways: - usually induce ROS production in cancer cells, while reducing ROS in normal cells. - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, - Lowers AntiOxidant defense in Cancer Cells: NRF2(typically increased), TrxR↓**, SOD↓, GSH↓ Catalase↓ HO1↓(wrong direction), GPx↓ - Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓ - inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓ - reactivate genes thereby inhibiting cancer cell growth : HDAC↓, EZH2↓, P53↑, HSP↓, Sp proteins↓, - cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓, - inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓, - inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, CD133↓, CD24↓, β-catenin↓, sox2↓, notch2↓, nestin↓, OCT4↓, - Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, - Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective, - Selectivity: Cancer Cells vs Normal Cells
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| Trimethylamine-N-oxide (TMAO) is a gut microbiota–derived metabolite produced from dietary precursors such as choline, phosphatidylcholine, and carnitine. In cancer, the current literature points to TMAO as generally pro-tumorigenic in several solid-tumor settings, especially colorectal cancer, hepatocellular carcinoma, and possibly prostate cancer, where it has been linked to higher proliferation, migration, angiogenesis, EMT, and inflammatory signaling. Mechanistically, reported pathways include VEGFA-driven angiogenesis, PI3K/AKT, MAPK, oxidative/inflammatory stress, and metabolic reprogramming. However, the picture is not uniformly one-directional: in some immune-competent models, particularly triple-negative breast cancer and pancreatic cancer, TMAO has been reported to enhance antitumor immunity and improve response to checkpoint blockade. So the fairest summary is that TMAO is usually associated with cancer-promoting biology in tumor-cell–centric studies, but can be context-dependent when the immune microenvironment is considered higher TMAO has been linked to several AD-relevant axes: neuroinflammation, vascular dysfunction, BBB/glymphatic impairment, oxidative stress, and amyloid/tau-associated pathology. -high concentrations of polyphenols (e.g., resveratrol, catechins, quercetin, and quercetin-3-O-glucoside), which act synergistically to protect various target organs from elevated TMAO levels -clinical studies demonstrated that high-dose atorvastatin (80 mg) or the combination of atorvastatin/ezetimibe or rosuvastatin can significantly reduce TMAO levels, likely due to their direct action on the TMAO-producing gut flora -Gut dysbiosis → TMA/TMAO production -Increase plant-forward foods and fiber to shift gut microbiota away from high TMA production. -TMAO is cleared renally and rises with kidney impairment. -"cold-pressed extra virgin olive oil and grape seed oil are rich in that 3,3-dimethyl-1-butanol (DMB). As a choline analog, DMB has been reported to be a broad-spectrum trimethylamine inhibitor, which has an obvious inhibitory effect on trimethylamine lyase in the intestinal flora, reducing the production of TMA and reducing the level of TMAO in vivo. In addition, resveratrol can reduce the plasma TMAO level by increasing the content of Lactobacillus and Bifidobacterium, and then reduce the occurrence and development of atherosclerosis" ref Dietary choline intake ∼ 350 mg/d was associated with the lowest risk of clinical diagnosis of AD in older adults. | Source | Typical serving | Choline/serving | Main choline form | TMAO relevance | | ---------------------- | --------------: | --------------: | ------------------- | ------------------------------------------ | | Egg yolk | 1 large yolk | ~125–150 mg | Phosphatidylcholine | High | | Whole egg | 1 large | ~145–150 mg | Phosphatidylcholine | High | | Beef liver | 3 oz | ~350+ mg | Mixed choline forms | High | | Chicken liver | 3 oz | ~240–290 mg | Mixed | High | | Salmon | 3 oz | ~70–90 mg | Mixed | Moderate; fish also contains TMAO directly | | Beef | 3 oz | ~70–110 mg | Choline + carnitine | High TMAO relevance | | Chicken breast | 3 oz | ~60–75 mg | Mixed | Moderate | | Soy lecithin | 1 tbsp, ~7–10 g | ~200–500 mg | Phosphatidylcholine | Moderate–high, depends on dose | | Sunflower lecithin | 1 tbsp, ~7–10 g | ~200–500 mg | Phosphatidylcholine | Moderate–high, depends on dose | | Egg lecithin | 1 tbsp, ~7–10 g | ~400–900 mg | Phosphatidylcholine | High | | High-PC lecithin | 1 g PC | ~130 mg choline | Phosphatidylcholine | High if taken daily | | Soybeans, cooked | ½ cup | ~100 mg | Mixed | Moderate | | Wheat germ | ¼ cup | ~50 mg | Mixed | Low–moderate | | Milk | 1 cup | ~35–45 mg | Mixed | Low–moderate | | Broccoli / cauliflower | 1 cup cooked | ~30–60 mg | Mixed | Low | | Potato | 1 medium | ~25–45 mg | Mixed | Low | |
| 6109- | statins, | RES, | Trimethylamine-N-Oxide (TMAO) as a Rising-Star Metabolite: Implications for Human Health |
| - | Review, | Nor, | NA |
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
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