3 replies to this topic

[sUper GeNius]

Sorry for this poopy post, but I'd like speak to the laxative effects of resveratrol. The 98% powder produces very large and regular bowl movements for me. I'm wondering whether this indicates increased water volume, together with rapid transit time.

If so, I wonder whether this effect, together with any positive effect t-res would have with its direct contact with digestive tract cells, would result in decreased rates of colon cancer?

[maxwatt]

Sorry for this poopy post, but I'd like speak to the laxative effects of resveratrol. The 98% powder produces very large and regular bowl movements for me. I'm wondering whether this indicates increased water volume, together with rapid transit time.

If so, I wonder whether this effect, together with any positive effect t-res would have with its direct contact with digestive tract cells, would result in decreased rates of colon cancer?

If you search pub med, you'll find numerous studies where resveratrol was a induced apoptosis in cancer cells in vitro. It does seem a promising potential therapy, but I think it has nothing to do with the laxative effects, which I find to be intermittent and dose dependant. This is due to increased chloride secretion by the intestines when exposed to resveratrol. A treatment we've discussed before, and which many of us find effective, is to drink a cup of a weak sugar solution/electrolyte replacement on an empty stomach. A recipe for this drink is to dissolve 2 teaspoons of sugar and one teaspoon of salt in a cup (8 ounces) of water. The salt may be optional, but replaces lost electrolytes.

[Hedgehog]

Sorry for this poopy post, but I'd like speak to the laxative effects of resveratrol. The 98% powder produces very large and regular bowl movements for me. I'm wondering whether this indicates increased water volume, together with rapid transit time.

If so, I wonder whether this effect, together with any positive effect t-res would have with its direct contact with digestive tract cells, would result in decreased rates of colon cancer?

There is a large article published a few days ago regarding Resveratrol Cancer & also talks about its chemopreventive aspects

http://www.ncbi.nlm....Pubmed_RVDocSum

A plant kingdom is considered as a gold mine for the discovery of many biologically active substances with therapeutic values. Resveratrol (3,5,4'-trihydroxystilbene), a naturally occurring polyphenol, exhibits pleiotropic health beneficial effects including anti-oxidant, anti-inflammatory, cardioprotective and anti-tumor activities. Currently, numerous preclinical findings suggest resveratrol as a promising nature's arsenal for cancer prevention and treatment. A remarkable progress in dissecting the molecular mechanisms underlying anti-cancer properties of resveratrol has been achieved in the past decade. As a potential anti-cancer agent, resveratrol has been shown to inhibit or retard the growth of various cancer cells in culture and implanted tumors in vivo. The compound significantly inhibits experimental tumorigenesis in a wide range of animal models. Resveratrol targets many components of intracellular signaling pathways including pro-inflammatory mediators, regulators of cell survival and apoptosis, and tumor angiogenic and metastatic switches by modulating a distinct set of upstream kinases, transcription factors and their regulators. This review summarizes the diverse molecular targets of resveratrol with a special focus on those involved in fine-tuning of orchestrated intracellular signal transduction.

I can post some snippets of this article if any body is interested???

[Hedgehog]

Molecular targets	Experimental models
AhR and CYP enzymes
↓AhR DNA binding; ↓expression and activity of CYP 1A1/1B1	TCDD-treated MCF-10A cells [22]
↓Expression and activity of CYP 1A1/1A2	B[a]P-treated HepG2 cells and DMBA-treated MCF-7 cells [26]
↓CYP 1A activity	Hepa1c1c7 cells [25]
↓CYP 1A1 and CYP1B1 activity	In vitro study using human liver microsomes [29]
↓Expression of CYP 1A1	B[a]P-treated mouse lung tissue [27]
↓CYP 19 (aromatase) activity	MCF-7 cells [30]
Direct interaction with CYP 19	Molecular modeling and docking study [31]
Phase II detoxification and antioxidant enzymes
↑NQO-1 activity	Hepa1c1c7 murine hepatoma cells [25]
↑Expression of protein and mRNA of NQO-1; ↑NQO-1 activity	Human K562 cells [36]
↑Gastrointestinal GPx promoter activity	HepG2 cells [35]
↑Expression of protein and mRNA and promoter activity of HO-1	Human aortic smooth muscle cells [34]
↑Expression of HO-1 protein and mRNA; ↑GCLC mRNA and GCLC promoter activity	PC12 cells [32]
↑Expression of GCL	CSE-treated SAEC and A549 cells [37]
Pro-inflammatory mediators
↓Mammary tumorigenesis; ↓COX-2	DMBA-induced rat mammary tumor and MCF-7 cells [152]
↓Esophageal tumors; ↓COX-1 and COX-2; ↓PGE2 level	NMBA-treated F344 male rats [49]
↓COX activity; ↓expression and activity of ODC	UVB-irradiated SKH hairless mouse skin [153]
↓COX-2 mRNA and protein level; ↓PGE2 level;	Human mammary and oral epithelial cells [52] and [147]
↓cox-2 promoter activity; ↓PKC activation; ↓AP-1 activity
↓Expression of iNOS and COX-2; ↓IκB degradation	LPS- or IFN-γ-stimulated Raw 264.7 cells [47]
↓Expression of COX-2, ↓IKK activity, ↓MAP kinase activation, ↓NF-κB and AP-1 DNA binding; ↓IκB phosphorylation and degradation, ↓p65 phosphorylation and nuclear translocation, ↓p65 and CBP interaction	Female ICR mouse skin treated with TPA [48] and [154]
↓NF-κB nuclear translocation; ↓NO production	Raw 264.7 and J774.2 cells treated with LPS [139]
↓IL-8 production; ↓AP-1 activity	TPA-treated Myeloid (U937) cells [57]
↓TNF- mRNA expression	LPS-treated J774.2 macrophages [54]
↓Serum levels of IL-6	Mice transplanted with L1210 cells [56]
Components of cell cycle machinery
↑p21 expression; G1 phase arrest	HepG2 cells [82]
↑p21WAF1/CIP1 expression, ↓cyclin D1/D2-Cdk6 and ↓cyclin D1/D2-Cdk4 complex formation	A431 cells [63]
↓Cyclin E-Cdk2 complex formation; ↓hyperphosphorylation of Rb; ↓free E2F	A431 cells [64]
↓Expression of cyclin B1, D1, A1 and β-catenin	SW480 cells [69]
↓Cyclin D1 and Cdk4 expression; ↑cyclin E and A expression; shifting of hyperphosphorylated Rb to hypophosphorylated form	Caco2 and HCT-116 cells [70]
↓ERK phosphorylation, ↓ expression of cyclin D1/D2	UVB-irradiated SKH-1 hairless mouse skin [65]
Causes G1 arrest, ↓cyclin A and D1, ↓Cdk-6, ↓ERK, ↓AP-1, ↑accumulation of hypophosphorylated Rb	A-431 cells [119]
Induces S phase arrest, ↑Cdc25c phosphorylation,	OVCAR-3 cells [71]
↑Chk1/2 expression, ↑ATM kinase activity
Molecules of the apoptotic signaling pathway
↑Expression of CD95L, ↑caspase-mediated PARP cleavage	HL-60 and T47D cells [75]
Redistribution of death receptors in membrane lipid rafts; ↑activation of caspases	SW480 cells [76] and [77]
↓Akt phosphorylation, stimulation of death receptors, ↑caspase activation	PC-3 and DU-145 cells [79]
↑Activation of ERK, p38 and JNK; ↑p53 phosphorylation	JB6 cells [86] and [87]
↑Expression of p53 responsive genes: p53,p21, p300/CBPand Apaf-1	LNCaP cells [85]
↑MAP kinases; ↑ phosphorylation of p53; ↑p53 DNA binding	DU-145 cells [115]
↓Bcl-2 expression; ↑Bax expression	Human esophageal cancer cells [155]
↑Bax expression; ↑activation of caspase 3 and 9	HCT-116 cells [84]
↑Cytochrome c release; activation of caspase-3	Human pancreatic cancer cells [156]
↑Caspase 2, ↑mitochondrial translocation of Bid, ↑AIF, ↑caspase-3 and -9	HCT-116 cells [88]
↑Nuclear co-localization of COX-2, p53 and CBP, ↑phosphorylation of p53	MCF-7 and MDA-MB-231 cells [91]
Direct binding to integrinVβ3, ↑p53-dependent apoptosis	MCF-7 cells [90]
↑Mitochondrial ROS, ↑phosphorylation of ERK and p38 MAP kinases, ↑p53 phosphorylation, ↑p21, ↑pChk1, ↑ATM kinase, ↑senescence-like growth arrest	HCT-116 cells [81]
↑Caspase-6-mediated cleavage of lamin A	HCT-116 (Bax+/−) cells [89]
↑Cytochrome c release, ↑cleavage of caspase-9 and-3, and PARP, ↑expression of p53, ↑Bax expression, ↑APAF-1, ↓Bcl-2	DMBA-TPA-induced mouse skin papillomas [74]
Molecular switches of angiogenic and metastatic progression
↓Secretion of VEGF	Human leukemia U937 cells [157]
↓Phosphorylation of ERK, ↓Expression of MMP-9	Heregulin-β1-treated MCF-7 cells [104]
↓Expression of MMP-9	DMBA-induced mouse mammary tumors [152]
↓Expression and activity of MMP-2 and -9	Multiple myeloma cells [103]
↓HIF-1 protein expression, ↓VEGF expression	A2780/CP70 and OVCAR-3 cells [72]
↓Extracellular levels of VEGF	MDA-MB-231 cells [12]
↓Expression of protein and mRNA of HIF-1 and VEGF	Human tongue squamous cell carcinomas and hepatoma cells [100]
↓HIF-1 and VEGF expression	LPA-treated ovarian cancer cells [101]