目的 研究姜黄素对脂多糖(LPS)诱导人脐静脉内皮细胞(HUVEC)炎症因子表达的影响,初步探讨可能的分子机制.方法 使用LPS(1μg)和姜黄素(5μmol/L、15μmol/L或30μmol/L)处理HUVEC细胞24 h,收集细胞总RNA,实时定量PCR(RT-PCR)和ELISA方法检测细胞TNF-α、MCP-1水平;Western blot检测细胞TLR4、MAPKs、NF-κB p65、磷酸化-NF-κB p65及NF-κB抑制蛋白IκBα的表达情况.结果 与空白对照组比较,姜黄素能显著抑制LPS诱导HUVEC细胞TNF-α、MCP-1和TLR4的过表达(P<0.05),明显降低NF-κB p65和MAPKs的磷酸化及IκBα蛋白降解(P<0.05).结论 姜黄素可能基于抑制TLR4/NF-κB,从而影响LPS诱导HUVEC细胞炎症因子的表达.%Objective To investigate the effect of curcumin on the expression of inflammatory response in-duced by lipopolysaccharide (LPS) in human umbilical vein endothelial cells (HUVEC) and to explore its molecular mechanisms. Methods The total RNA was extracted from HUVEC treated with LPS (1μg/L) and curcumin (5, 15, or 30μmol/L) for 24 h. The levels of tumor necrosis factor-α(TNF-α) and monocyte chemoattractant protein-1 (MCP-1) were detected using real-time reverse transcriptase polymerase chain reaction (RT-PCR) and enzyme-linked immuno-sorbent assay (ELISA). Western blot was used to detect the activation of Toll like receptor 4 (TLR4), mitogen-activated protein kinases (MAPKs), nuclear factor kappa B (NF-κB) p65, phosphor-NF-κB p65 and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκBα) in the cells. Results Compared with the untreated cells, curcumin significantly inhibited the overexpression of TNF-α, MCP-1 and TLR4 in HUVEC cells induced by LPS (P<0.05), which also significantly reduced NF-κB p65 and MAPKs phosphorylation and IκBαprotein degrada-tion. Conclusion Curcumin suppresses LPS-induced inflammatory response in HUVEC in vitro via inhibiting the TLR4/NF-κB pathways.
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