中文摘要：

目的：探讨小鼠急性心肌梗死（AMI）后炎症因子IL-1β和IL-6的动态变化及3-甲基腺嘌呤对心肌炎症因子IL-1β和IL-6释放的影响。方法：雄性C57BL/6小鼠随机分成四组：假手术组、AMI 1 d组、AMI 7 d组、AMI 21 d组,用超声心动仪检测心功能变化,用荧光定量PCR法、ELISA法和免疫组化法测量血清和心肌组织中炎症因子IL-1β和IL-6的变化,用免疫蛋白印迹方法检测心肌组织IL-1β转换酶caspase-1蛋白的变化情况。在AMI后给予3-甲基腺嘌呤7 d,用超声心动仪检测心功能变,用ELISA法和免疫组化法测量心肌组织中炎症因子IL-1β和IL-6的变化情况。结果：小鼠冠状动脉左前降支结扎术后7、21 d心功能显著下降。小鼠AMI后炎症因子IL-1β和IL-6的mRNA水平表达增加,在血清和心肌组织中蛋白含量增加（P〈0.05）。小鼠AMI后心肌中caspase-1蛋白表达增加（P〈0.05）。3-甲基腺嘌呤加重小鼠AMI 7 d后心脏功能下降（P〈0.05）,并促进炎症因子IL-1β和IL-6的释放（P〈0.05）。结论：小鼠心肌损伤过程中炎症因子IL-1β和IL-6表达增加,其机制可能跟AMI后caspase-1的增加有关;3-甲基腺嘌呤加重AMI后心功能的下降,其机制可能与促进炎症因子释放有关。

英文摘要：

Objective： To investigate the dynamic changes of the inflammatory cytokines,interleukin-1β（ IL-1β） and IL-6 in mice after acute myocardial infarction（ AMI） and the effect of 3-methyl adenine on the release of myocardial inflammatory cytokines IL-1β and IL-6. Methods： Male C57 BL /6 mice were randomly divided into four groups： sham operation group,AMI 1 day（ AMI 1d） group,AMI 7 days（ AMI 7d） group,and AMI 21 days（ AMI 21d） group. We determined the changes of heart function by echocardiography,the changes of inflammatory cytokines IL-1β and IL-6 in serum and myocardial tissue by fluorescent quantitative polymerase chain reaction（ FQ-PCR）,enzyme-linked immuno sorbent assay（ ELISA） and immunohistochemistry,and IL-1β converting enzyme caspase-1 protein in myocardial tissue by Western blotting. All mice were given 3-methyl adenine for seven days after AMI. We determined the changes of heart function by echocardiography,the changes of inflammatory cytokines IL-1β and IL-6 in myocardial tissue by ELISA and immunohistochemistry. Results：The heart function in mice was significantly decreased at 7 and 21 d after left anterior descending coronary artery ligation. Increased mRNA expression levels of inflammatory cytokines IL-1β and IL-6,and increased protein levels in serum and myocardial tissue were found in mice after AMI（ P 〈 0. 05）. The caspase-1 protein expression was increased in myocardial tissue in mice after AMI（ P 〈 0. 05）. 3-methyl adenine aggravated heart dysfunction in the AMI 7d group（ P 〈 0. 05）,and promoted the release of inflammatory cytokines IL-1β and IL-6（ P 〈 0. 05）. Conclusion： In the process of myocardial injury,inflammatory cytokines IL-1β and IL-6expression are increased in mice. The mechanism may be associated with the increased caspase-1 after AMI. 3-methyl adenine aggravates heart dysfunction in mice after AMI, probably via the release of inflammatory cytokines.