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deserusan's Stats for More on the Cissus + Arachidonic Acid Debate
Created:10/05/2007
Last Modified:10/05/2007
Total Comments:0



More on the Cissus + Arachidonic Acid Debate

Quote:
Originally Posted by getbustered
I don’t think you are a bad bro at all, and I don’t think there is anything wrong with this thread. I DO hope that it doesn’t turn into bad blood between anyone in the future, but only time will tell that. In the end, this has been an informative thread; and how many threads these days feature an appearance from Bill and Phosphate? That is notable in itself.

There isn’t any bad blood nor will there be. Obviously, since a similiar supplement has been marketed my attention will certainly be drawn to this and questions will follow.

You have to understand that despite not being expert in anything I do field hundreds of questions a week regarding compounds like these. Will this stack well with that? Will product X interfere with product Y and so and so forth. Despite obvious biases I try to form my responses to give the best possible answer regardless of affiliation. I pride myself on this ability.

With that said, I do firmly believe there is a contradiction between AA and CQ. Stacking the two renders one or both compounds useless for their intended purpose regardless of dosing (this dictates effectiveness). My own personal use and all the availably research seems to ellucidate this fact. I have nothing else to base my opinion on as user feedback is generally skewed. Here is some great research as to why:

McClung M, Collins D. “Because I know it will!”: placebo effects of an ergogenic aid on athletic performance. J Sport Exerc Psychol. 2007 Jun;29(3):382-94.Beedie CJ, Coleman DA, Foad AJ. Positive and negative placebo effects resulting from the deceptive administration of an ergogenic aid. Int J Sport Nutr Exerc Metab. 2007 Jun;17(3):259-69.

This wasn’t meant to be a pissing contest, but some parties failed miserably in providing insight. Obviously, yohimbine can take care of any doubts consumers may have these days about the effectiveness of their supplements. It sadly makes me wonder why I spend so much time doing research on my own free will.

Quote:
Nat Prod Res. 2007 May 20;21(6):522-8. 

Constituents of Cissus quadrangularis.Singh G, Rawat P, Maurya R.

Medicinal and Process Chemistry Division, Central Drug Research Institute, Lucknow, India.

Two new iridoids 6-O-[2,3-dimethoxy]-trans-cinnamoyl catalpol (1) and 6-O-meta-methoxy-benzoyl catalpol (2) along with a known iridoid picroside 1 (3), two stilbenes quadrangularin A (4) and pallidol (5), quercitin (6), quercitrin (7), beta-sitosterol (8) and beta-sitosterol glycoside (9) were isolated from Cissus quadrangularis Linn. The compounds 3 and 7 are first reported from this plant. The structures were elucidated by analysis of their spectroscopic data and by direct comparison with literature. This is the first reported occurrence of iridoids in C. quadrangularis.

Iridoids are known COX II inhibitors showing preferential inhibition over COX I and LOX. Granted, I’m basing my opinion on the in vitro studies with iridoids isolated from a different genus of plant. However, this could in part explain some of the anti-inflammatory action of cissus via the COX-II pathway.

Quote:
Biological and pharmacological activities of iridoids: recent developments.Rosa Tundis, Monica R. Loizzo, Federica Menichini, Giancarlo A. Statti,Francesco Menichini 

Department of Pharmaceutical Sciences, Faculty of Pharmacy Nutrition and Health Sciences, University of Calabria, 87036-I Rende (CS), Italy

http://64.233.167.104/search?q=cache…RMC-132660.pdf

Quote:
Originally Posted by Dr.P
nice find on the iridoids. just be aware that there is a large variety of different iridoid derivatives that may have different effects. catalpol, for example has been shown to inhibit iNOS and TNF-alpha and to reduce ROS. other iridoids have been found to act on COX, while again some others have been found to affect LOX and IL1-beta.

True. This whole debate has certainly rekindled my interest in cissus and luckily there is a little bit more research since I last took a close look at it. It’s funny you mention catapol inhibition of TNF-alpha. That cascade could potentially prevent atrophy in the short term. However, NF-kappaB is mediated downstream of TNF-alpha so inhibition of this pathway in myocytes can be caused by quercitrin, also a component of cissus.

Quote:
EurJ Immunol. 2005 Feb;35(2):584-92. 

In vivo quercitrin anti-inflammatory effect involves release of quercetin, which inhibits inflammation through down-regulation of the NF-kappaB pathway.

Comalada M, Camuesco D, Sierra S, Ballester I, Xaus J, G?lvez J, Zarzuelo A.

Department of Pharmacology, University of Granada, Granada, Spain.

Quercetin is a common antioxidant flavonoid found in vegetables, which is usually present in glycosylated forms, such as quercitrin (3-rhamnosylquercetin). Previous in vitro experiments have shown that quercetin exerts a bigger effect than quercitrin in the down-regulation of the inflammatory response. However, such results have not been reproduced in in vivo experimental models of intestinal inflammation, in which quercetin did not show beneficial effects while its glycosides, quercitrin or rutin, have demonstrated their effectiveness. In this study, we have reported that the in vivo effects of quercitrin in the experimental model of rat colitis induced by dextran sulfate sodium can be mediated by the release of quercetin generated after glycoside’s cleavage by the intestinal microbiota. This is supported by the fact that quercetin, but not quercitrin, is able to down-regulate the inflammatory response of bone marrow-derived macrophages in vitro. Moreover, we have demonstrated that quercetin inhibits cytokine and inducible nitric oxide synthase expression through inhibition of the NF-kappaB pathway without modification of c-Jun N-terminal kinase activity (both in vitro and in vivo). As a conclusion, our report suggests that quercitrin releases quercetin in order to perform its anti-inflammatory effect which is mediated through the inhibition of the NF-kappaB pathway.

At least this isn’t via COX II which would inbihibit PGE2alpha and the welcome effects of AA due the inflammation response to eccentric motion involved in hypertrophy.

Inhibition of NF-KappaB itself it a tricky one to figure out. It is responsible for regulation of various genes involved with cell growth, death, and immune responses in skeletal muscle. This is why I was never a fan of long term use of certain compounds which inhibit NF-KappaB multiple times a day. You are just beating down an important pathway.

Quote:
NF-kappa B mediates the protein loss induced by TNF-alpha in differentiated skeletal muscle myotubes 

Yi-Ping Li and Micheal B. Reid

Department of Medicine, Baylor College of Medicine, Houston, Texas 77030

Nuclear factor-kappa B (NF-kappa B) regulates the transcription of a variety of genes involved in immune responses, cell growth, and cell death. However, the role of NF-kappa B in muscle biology is poorly understood. We recently reported that tumor necrosis factor-alpha (TNF-alpha ) rapidly activates NF-kappa B in differentiated skeletal muscle myotubes and that TNF-alpha acts directly on the muscle cell to induce protein degradation. In the present study, we ask whether NF-kappa B mediates the protein loss induced by TNF-alpha . We addressed this problem by creating stable, transdominant negative muscle cell lines. C2C12 myoblasts were transfected with viral plasmid constructs that induce overexpression of mutant I-kappa Balpha proteins that are insensitive to degradation via the ubiquitin-proteasome pathway. These mutant proteins selectively inhibit NF-kappa B activation. We found that differentiated myotubes transfected with the empty viral vector (controls) underwent a drop in total protein content and in fast-type myosin heavy-chain content during 72 h of exposure to TNF-alpha . In contrast, total protein and fast-type myosin heavy-chain levels were unaltered by TNF-alpha in the transdominant negative cell lines. TNF-alpha did not induce apoptosis in any cell line, as assessed by DNA ladder and annexin V assays. These data indicate that NF-kappa B is an essential mediator of TNF-alpha -induced catabolism in differentiated muscle cells.

The forum needs more discussion like this. Anyway, my own use of cissus has been brief and when certain joint issues flare up. I don’t like the idea of using analgesics when not needed even if they have shown to be friendly to the GI tract unlike NSAIDs.

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