Dr. Tobinick could have solved this TNF question years ago if he had only actually run clinical tests on etanercept.
http://www.sciencedirect.com/science/article/pii/S0367326X16301150
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Inflammatory
response plays an important role in the activation and progress of many
debilitating diseases. Natural products, like cannabidiol, a
constituent of Cannabis sativa, and moringin, an isothiocyanate
obtained from myrosinase-mediated hydrolysis of the glucosinolate
precursor glucomoringin present in Moringa oleifera seeds, are well known antioxidants also endowed with anti-inflammatory
activity. This is due to a covalent-based mechanism for ITC, while
non-covalent interactions underlie the activity of CBD. Since these two
mechanisms are distinct, and the molecular endpoints are potentially
complementary, we investigated in a comparative way the protective
effect of these compounds alone or in combination on
lipopolysaccharide-stimulated murine macrophages. Our results show that
the cannabidiol (5 μM) and moringin (5 μM) combination outperformed the
single constituents that, at this dosage had only a moderate efficacy on
inflammatory (Tumor necrosis factor-α, Interleukin-10) and oxidative
markers (inducible nitric oxide synthase, nuclear factor erythroid
2-related factor 2, nitrotyrosine). Significant upregulation of Bcl-2
and downregulation of Bax and cleaved caspase-3 was observed in cells
treated with cannabidiol-moringin combination. Treatment with the
transient receptor potential vanilloid receptor 1 antagonist was
detrimental for the efficacy of cannabidiol, while no effect was
elicited by cannabinoid receptor 1 and cannabinoid receptor 2
antagonists. None of these receptors was involved in the activity of
moringin. Taken together, our in vitro results testify the anti-inflammatory, antioxidative, and anti-apoptotic effects of the combination of cannabidiol and moringin.
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