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机构地区:[1]浙江中医药大学附属第一医院检验科,浙江杭州310006
出 处:《中国微生态学杂志》2015年第8期900-903,共4页Chinese Journal of Microecology
基 金:浙江省中医药科技计划一般项目(2013ZA044)
摘 要:目的探讨姜黄素对LPS诱导的大鼠肠黏膜微血管内皮细胞表达COX-2的影响及机制。方法选用大鼠肠黏膜微血管内皮细胞,随机分组,用p38MAPK抑制剂、PPARγ拮抗剂、姜黄素进行干预。荧光定量RT-PCR检测COX-2 mRNA的表达量,WB法检测其相关蛋白。结果LPS组较正常对照组COX-2增高3.5倍,差异有统计学意义(P<0.01)。姜黄素组、p38MAPK选择性抑制剂组、PPARγ拮杭剂组较LPS组,COX-2明显降低。阻断p38MAPK后,COX-2蛋白表达下降。姜黄素可以增加PPARγ、COX-2、p-p38的表达。结论姜黄素可降低COX-2表达水平,p38MAPK、PPARγ通路参与姜黄素调控COX-2的表达。Objective To explore the effects of curcumine on the expression of COX-2induced by LPS in vascular endothelial cells.Methods The endothelial cells of rats were randomly individed into seven groups,and intervened with P38 inhibitor,PPARγantagonist and curcumine respectively.The expression of COX-2mRNA was detected by real-time reverse transcription polymerase chain reaction(PCR).Results The COX-2level in LPS group was significantly higher than those in the control groups(P〈0.01);The COX-2levels in the p38 MAPK,PPARγantagonist and curcumine groups were obviously lower than that in the LPS group.Conclusion Curcumine can reduce the expression level of COX-2.The signal pathways of p38 MAPK and PPARγplay important roles in the regulation of COX-2expression by curcumine.
关 键 词:肠黏膜微血管内皮细胞 姜黄素 环氧化酶-2
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