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首页> 外文期刊>Die Pharmazie >Vitamin D suppresses lipopolysaccharide-induced inflammatory response in vascular smooth muscle cells via inhibition of the p38 MAPK signaling pathway
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Vitamin D suppresses lipopolysaccharide-induced inflammatory response in vascular smooth muscle cells via inhibition of the p38 MAPK signaling pathway

机译:维生素D通过抑制P38 MAPK信号通路抑制血管平滑肌细胞中的脂多糖诱导的炎症反应

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摘要

Inflammation and vascular smooth muscle cells (VSMCs) play key roles in the development of many cardiovascular diseases (CVDs). Although vitamin D decreases the risks of inflammation related diseases including CVDs, the links between vitamin D, VSMCs and vascular inflammation remainedunclear. In this study, we investigated the anti-inflammatory effect and signaling pathways of vitamin D in lipopolysaccharide (LPS)-induced VSMCs. 1,25(OH)2D3 treatment inhibited the significant upregulation of COX-2, PGE2, TNF-α and IL-6 and p38 phosphorylationinduced by LPS in A10 cells. Blocking p38 signaling attenuated the inhibitory effect of 1,25(OH)2D3 on the upregulation of COX-2 and phosphorylation of p38. These results indicate 1,25(OH)2D3 suppresses inflammatory response in LPS-induced VSMCsthrough p38 MAPK signaling pathway.
机译:炎症和血管平滑肌细胞(VSMCS)在许多心血管疾病(CVDS)的发展中起关键作用。 虽然维生素D降低了炎症相关疾病的风险,包括CVD,维生素D,VSMC和血管炎症之间的联系。 在这项研究中,我们研究了脂多糖(LPS)诱导的VSMC中维生素D的抗炎作用和信号通路。 1,25(OH)2D3处理抑制了通过LPS在A10细胞中的LPS的COX-2,PGE2,TNF-α和IL-6和P38磷化的显着上调。 阻断P38信号传导衰减1,25(OH)2D3对COX-2的上调和P38磷酸化的抑制作用。 这些结果表明1,25(OH)2D3抑制LPS诱导的VSMCSTHROUGH P38 MAPK信号通路中的炎症反应。

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