Paeonol attenuates advanced oxidation protein product-induced oxidative stress injury in THP-1 macro

来源 :2014年中国药学大会暨第十四届中国药师周 | 被引量 : 0次 | 上传用户:narco008
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  Ethnopharmacological relevance: Paeonol (2′-hydroxy-4′methoxyacetophenone),is thought to possess a broad range of clinical curative effects that are likely mediated by its anti-inflammatory and anti-oxidant activities.Aims of the study: To elucidate the efficacy of paeonols anti-inflammatory and anti-oxidant activities and the underlying mechanism of paeonol in AOPP (advanced oxidation protein product)-stimulated THP-1 macrophages.Materials and methods: After incubating the cells with AOPP plus paeonol,nitric oxide (NO) production and the levels of iNOS,RAGE (Receptor for advanced glycation end products),CD36,SR-A,SR-B1 were calculated.Moreover,THP-1 macrophages were pre-incubated with paeonol,a free radical scavenger N-acetylcysteine (NAC),NADPH oxidase inhibitor (apocynin,DPI),a specific inhibitor of nuclear factor kappa-B (NF-κB) pyrrolidine dithiocarbamate (PDTC,) prior to incubation with AOPP,then intracellular ROS (reactive oxygen species) production and quantification of tumor necrosis factor-α (TNF-α),interleukin-1β (IL-1β),interleukin-6 (IL-6),MCP-1(monocyte chemotactic protein 1) were determined.Results: Paeonol increased NO production and the mRNA level of iNOS (inducible nitric oxide synthase),whereas decreased ROS production.ROS production was also effectively attenuated by apocynin,DPI,NAC and PDTC.Furthermore,these inhibitors and paeonol could down-regulate pro-inflammatory cytokine (TNF-α,IL-1β,IL-6 and MCP-1) mRNA and protein levels.Paeonol significantly reduced RAGE and CD36 gene expressions but increased SR-A and SR-B1 gene expressions.Conclusions: These results indicate that Paeonol could decrease inflammation cytokines in THP-1 macrophages likely through a RAGE,CD36,SR-A and SR-B1-mediated signals involving NADPH oxidase dependent ROS generation.This suggests that paeonol might be using as a therapeutic agent for the diseases contributed to oxidative stress injury.
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