【摘要】 目的探讨EAM小鼠血管紧张素Ⅱ(ATⅡ)水平及其在EAM发生中的作用。方法首先诱导EAM模型,ELISA检测ATⅡ的表达水平,然后实验分为对照组、EAM组、EAM+氯沙坦(ATⅡ抑制剂)组,第21天处死小鼠,HE染色观察心肌炎症浸润情况;RT-q PCR检测心脏组织中相关炎症因子(IL-1β、IL-6、TGF-β)的m RNA的表达水平;Transwell实验检测ATⅡ对巨噬细胞迁移作用及氯沙坦的抑制作用。结果成功诱导小鼠心肌炎模型,心肌组织中有大量的淋巴细胞浸润,ATⅡ水平增高,具有促进炎症因子释放及巨噬细胞迁移的作用;使用ATⅡ抑制剂氯沙坦治疗后,心肌组织炎症评分降低,减少了淋巴细胞浸润;IL-1β、IL-6水平降低,而抑炎因子TGF-β表达高于EAM组;ATⅡ对巨噬细胞的迁移作用受到抑制。结论 ATⅡ可能是EAM发生的重要因素,抑制ATⅡ能够有效缓解心肌炎症损伤。更多还原

【Abstract】 The study designed to detect the expression of angiotensin Ⅱ(ATⅡ)in experimental autoimmunemyocarditis(EAM)mice,and explore the role of ATⅡ in the occurrence of EAM.Firstly,EAM model were inducedand constructed.Then,mice were divided into control group,EAM group,and EAM+losartan group.Twenty-onedays after,the mice was sacrificed.The lymphocytes infiltration of model mice was detected by HE staining,them RNA levels of IL-1β,IL-6 and TGF-β were assayed by RT-q PCR,and the ATⅡ expression was assayed byELISA.Transwell was applied to assay the migration ability of macrophages.Data showed ATⅡ expression wasup-regulated in EMA mice,demonstrating the function of promoting the release of inflammatory factors and themigration of macrophages.Losartan(ATⅡ inhibitor)attenuated myocarditis,reduced lymphocyte infiltration,andinhibited the macrophage migration in EAM mice.Furthermore,the expression of IL-1 and IL-6 in losartantreatment group was lower than that of EAM group,but the expression of TGF-β was higher than EAM group.Inconclusion,AT Ⅱ might be contribute EAM development,and AT Ⅱ blockage would attenuate the myocarditisdevelopment.更多还原