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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。
Objective: To investigate the dynamic changes of inflammatory cytokines IL-1β and IL-6 after acute myocardial infarction (AMI) in mice and the effects of 3-methyladenine on the release of myocardial inflammatory cytokines IL-1β and IL-6. Methods: Male C57BL / 6 mice were randomly divided into four groups: sham operation group, AMI 1 d group, AMI 7 d group and AMI 21 d group. The changes of cardiac function were detected by echocardiography. Fluorescent quantitative PCR, ELISA and The changes of IL-1β and IL-6 in serum and myocardium were measured by immunohistochemistry. The changes of IL-1β-converting enzyme caspase-1 protein in myocardium were detected by Western blotting. After AMI, 3-methyladenine was given for 7 days. The changes of cardiac function were detected by echocardiography. The changes of inflammatory cytokines IL-1β and IL-6 in myocardium were measured by ELISA and immunohistochemistry. Results: The cardiac function of the left anterior descending coronary artery was significantly decreased at 7 and 21 d after coronary artery occlusion. After AMI, the mRNA expression of IL-1β and IL-6 increased, and the content of protein in serum and myocardium increased (P <0.05). The expression of caspase-1 in myocardium increased after AMI in mice (P <0.05). 3-methyladenine increased the cardiac function (P <0.05) and promoted the release of inflammatory cytokines IL-1β and IL-6 after 7-day AMI in mice (P <0.05). CONCLUSION: The expression of IL-1β and IL-6 may play an important role in the process of myocardial injury. The mechanism may be related to the increase of caspase-1 after AMI. The mechanism may be related to the decrease of cardiac function after 3-methyladenine exacerbation And promote the release of inflammatory cytokines.