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liver toxicity and glutathione disulfide sensitizes hepatocytes to TNFα-mediated cytotoxicity via IKK-β S-glutathionylation: a potential mechanism underlying non-alcoholic fatty disease idler-pulley
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liver toxicity and glutathione disulfide sensitizes hepatocytes to TNFα-mediated cytotoxicity via IKK-β S-glutathionylation: a potential mechanism underlying non-alcoholic fatty disease idler-pulley
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liver toxicity and glutathione disulfide sensitizes hepatocytes to TNFα-mediated cytotoxicity via IKK-β S-glutathionylation: a potential mechanism underlying non-alcoholic fatty disease idler-pulley
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liver toxicity and glutathione disulfide sensitizes hepatocytes to TNFα-mediated cytotoxicity via IKK-β S-glutathionylation: a potential mechanism underlying non-alcoholic fatty disease idler-pulley
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In an in vitro study on microglial cells, PYC dose-dependently decreased the release of nitric oxide, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1β, ICAM-1, and perilipin 2, thereby exhibiting anti-inflammatory activity ( Ex vivo analysis of plasma from volunteers following PYC administration revealed moderate inhibition of COX-1 and COX-2 activity, indicating potential anti-inflammatory and platelet-inhibitory effects (Schäfer et al., 2006)
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liver toxicity and glutathione disulfide sensitizes hepatocytes to TNFα-mediated cytotoxicity via IKK-β S-glutathionylation: a potential mechanism underlying non-alcoholic fatty disease idler-pulley
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