黑色素瘤缺乏因子2炎性小体在心肌梗死后心肌纤维化中的作用

The role of the absent in melanoma 2 inflammasome in myocardial fibrosis after myocardial infarction

目的探讨黑色素瘤缺乏因子2(AIM2)炎性小体在心肌梗死后心肌纤维化中的潜在作用。方法分别将Aim2^-/-及其同窝野生型(W T)小鼠行冠状动脉左前降支结扎法制备心肌梗死后心肌纤维化小鼠。记录4周内小鼠存活率,4周后心脏超声检测左室射血分数和心排血量,Masson染色检测心肌纤维化,蛋白印迹(W esternBlot,WB)技术检测心肌梗死后组织AIM2、TGF β,WB和组织免疫荧光检测心肌组织IL-1β和CollagenⅠ的表达。结果与野生型小鼠相比,Aim2^-/-小鼠心肌梗死后存活率和心脏功能(左室射血分数和心排血量)改善(P<0.05)、心肌纤维化程度减轻,心肌梗死后心肌纤维化组织CollagenⅠ、IL-1β、TGF-β等表达降低。结论 AIM2炎性小体是心肌梗死后心肌纤维化的重要调控分子。仍需要进一步探讨AIM2炎性小体调控心肌梗死后心肌纤维化的分子机制。

Objective To investigate the potential role of absent in melanoma 2(AIM2)inflammasome in myocardial fibrosis after myocardial infarction.Methods Aim2-/-mice and its littermate wild type mice(WT)underwent left anterior descending coronary artery ligation to prepare mice with myocardial fibrosis after myocardial infarction. The survival rate of mice was recorded within 4 weeks. After 4 weeks,left ventricular ejection fraction and cardiac output were measured by echocardiography;myocardial fibrosis was detected by Masson staining;the expression of AIM2,TGF-β was detected by western blotting;and the expression of Collagen I and IL-1β was detected by western blot and tissue immunofluorescence.Results Compared with wild type mice,Aim2-/-mice had better survival rate and cardiac function(left ventricular ejection fraction and cardiac output)after myocardial infarction(P < 0.05),less myocardial fibrosis and lower expression of Collagen Ⅰ,IL-1β and TGF-β in myocardial fibrosis tissue after myocardial infarction.Conclusion AIM2 inflammasome is an important regulator of myocardial fibrosis after myocardial infarction. The molecular mechanism of AIM2 inflammasome regulating myocardial fibrosis after myocardial infarction still needs to be further explored.