| 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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| SP2 (Specificity Protein 2) and SP3 (Specificity Protein 3) are also members of the Sp/KLF (Sp1/Krüppel-like factor) family of transcription factors, similar to SP1. They share some functional similarities but also have distinct roles in cellular processes and cancer biology. -Sp proteins are a family of transcription factors that play a crucial role in regulating gene expression. -SP1 is often overexpressed in various types of cancer, including breast, prostate, and lung cancers. However, expression levels of Sp in normal cells and tissues are low to undetectable. SP inhibitors: -Curcumin, Resveratrol, EGCG, Genistein, Piperlongumine, Betulinic acid |
| 3079- | RES, | Therapeutic role of resveratrol against hepatocellular carcinoma: A review on its molecular mechanisms of action |
| - | Review, | Var, | NA |
| 2981- | RES, | Resveratrol suppresses IGF-1 induced human colon cancer cell proliferation and elevates apoptosis via suppression of IGF-1R/Wnt and activation of p53 signaling pathways |
| - | in-vitro, | Colon, | HT-29 | - | in-vitro, | Colon, | SW48 |
| 2991- | RES, | Chemo, | Synergistic anti-cancer effects of resveratrol and chemotherapeutic agent clofarabine against human malignant mesothelioma MSTO-211H cells |
| - | in-vitro, | Melanoma, | MSTO-211H | - | in-vitro, | Nor, | MeT5A |
| 2990- | RES, | Resveratrol reduces cerebral edema through inhibition of de novo SUR1 expression induced after focal ischemia |
| - | in-vivo, | Stroke, | NA |
| 2989- | RES, | Resveratrol Represses Pokemon Expression in Human Glioma Cells |
| - | in-vitro, | GBM, | NA |
| 2988- | RES, | The Antimetastatic Effects of Resveratrol on Hepatocellular Carcinoma through the Downregulation of a Metastasis-Associated Protease by SP-1 Modulation |
| - | in-vitro, | HCC, | HUH7 |
| 2985- | RES, | Resveratrol Inhibits Diabetic-Induced Müller Cells Apoptosis through MicroRNA-29b/Specificity Protein 1 Pathway |
| - | in-vivo, | Nor, | NA | - | vitro+vivo, | Diabetic, | NA |
| 2984- | RES, | Involvement of miR-539-5p in the inhibition of de novo lipogenesis induced by resveratrol in white adipose tissue |
| - | in-vivo, | Nor, | NA |
| 2983- | RES, | Resveratrol Improves Diabetic Retinopathy via Regulating MicroRNA-29b/Specificity Protein 1/Apoptosis Pathway by Enhancing Autophagy |
| - | in-vitro, | Nor, | NA |
| 2982- | RES, | The flavonoid resveratrol suppresses growth of human malignant pleural mesothelioma cells through direct inhibition of specificity protein 1 |
| - | in-vitro, | Melanoma, | MSTO-211H |
| 104- | RES, | QC, | Resveratrol and Quercetin in Combination Have Anticancer Activity in Colon Cancer Cells and Repress Oncogenic microRNA-27a |
| - | in-vitro, | Colon, | HT-29 |
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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