MAPK信号通路在肺炎衣原体感染小鼠中作用.docVIP

MAPK信号通路在肺炎衣原体感染小鼠中作用 　　[摘要] 目的 研究MAPK信号通路在肺炎衣原体（CP）感染APOE基因敲除（APOE）小鼠促进动脉粥样硬化形成中的作用。 方法 48只APOE小鼠分为感染-高脂组、高脂组、感染组和对照组，每组12只，喂养20周，采用Western blot和Real time-PCR法检测胞外信号调控激酶（p-ERK1/2）、p-P38的蛋白表达和白介素-6（IL-6）、肿瘤坏死因子（TNF-α）的基因的表达。 结果 感染-高脂组、高脂组、感染组APOE小鼠的主动脉IL-6和TNF-α水平明显高于对照组（P 0.05）。与对照组比较，感染-高脂组、高脂组、感染组p-ERK1/2、p-P38蛋白表达的水平显著降低（P 0.05）。 结论 CP感染激发和加重动脉内炎性反应可促进动脉粥样硬化，MAPK信号通路是CP促进动脉粥样硬化的潜在机制。 　　[关键词] 动脉粥样硬化；白介素-6；丝裂原活化蛋白激酶 　　[中图分类号] R543.5 [文献标识码] A [文章编号] 1673-7210（2015）09（a）-0015-05 　　[Abstract] Objective To investigate the role of MAPK in APOE mice induced atherosclerosis （AS） by chlamydia pneumoniae （CP） infection. Methods Forty-eight APOE mice were divided into four groups including CP infection and hyperlipidemia group， hyperlipidemia group， CP infection group and control group， each group had 12 mice. The mice were sacrificed at 20 week of age. Western blot and Real time-PCR were used to detect the p-ERK1/2， p-P38 protein expression and the gene expression of IL-6， TNF-α. Results The levels of IL-6 and TNF-α in CP infection and hyperlipidemia group， hyperlipidemia group， CP infection group were significantly higher than those in control group， the differences were statistically significant （P 0.05）. Compared with the control group， the levels of p-ERK1/2， p-P38 protein expression in CP infection and hyperlipidemia group， hyperlipidemia group， CP infection group significantly reduced， with statistically significant differences （P 0.05）. Conclusion Infection with CP may contribute to AS by the initiation and progression of the inflammatory reaction within the artery. MAPK is a potential mechanism of CP induced AS. 　　[Key words] Atherosclerosis； IL-6； MAPK 　　当今心脑血管疾病的发病率呈现逐年上升的趋势，随着全球人口老龄化的进程和生活饮食习惯的改变，发病人群有逐年增加和年轻化的趋势[1-2]。动脉粥样硬化（atherosclerosis，AS）作为心脑血管疾病的病变基础，其发病机制至今仍不明确[3-5]。近年来国内外一些研究发现，肺炎衣原体（chlamydia pneumoniae，CP）感染可能参与动脉粥样硬化病变的发生、发展过程[6]。 　　丝裂原活化蛋白激酶（mitogen-activated protein kinases，MAPK）是细胞内的一类丝氨酸/苏氨酸蛋白激酶。MAPK信号通路在调控心血管疾病的研究中日益受到人们的重视。笔者以往研究已经