瘦素预处理诱导心肌细胞自噬减轻心肌缺血再灌注损伤  

Leptin preconditioning alleviates myocardial ischemia/reperfusion injury by inducing autophagy of cardiomyocytes

作　　者：朱盼盼 徐彤彤[1] 覃秋语 彭丽[1] Zhu Panpan;Xu Tongtong;Qin Qiuyu;Peng Li(Department of Health Care Ward,Affiliated Hospital of Guilin Medical College,Guilin 541001,Guangxi Zhuang Autonomous Region,China)

机构地区：[1]桂林医学院附属医院综合科(医疗保健病区),541001

出　　处：《中华老年心脑血管病杂志》2021年第12期1309-1312,共4页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

基　　金：国家自然科学基金(81760861)。

摘　　要：目的研究瘦素预处理对心肌缺血再灌注损伤(myocardial ischemia reperfusion injury, MIRI)模型SD大鼠心肌细胞自噬的影响。方法将18只成年雄性SD大鼠随机分为假手术组、模型组和预处理组,每组6只。假手术组仅开胸不结扎血管;模型组和预处理组大鼠用绳栓法建立MIRI模型;预处理组建模前行瘦素预处理;用TTC染色检测心肌梗死面积,苏木精-伊红染色检测心肌损伤程度,采用Western blot法检测大鼠心肌P62和自噬微管相关蛋白轻链3(LC3B)蛋白表达。结果与假手术组比较,模型组和预处理组大鼠心肌梗死面积增大,心肌损伤评分升高(P<0.05),模型组大鼠P62蛋白表达显著升高,LC3B蛋白表达显著降低;预处理组大鼠心肌组织P62蛋白和LC3B蛋白表达均升高。与模型组比较,预处理组大鼠心肌梗死面积缩小[(17.83±1.86)%vs(32.33±2.29)%],心肌损伤评分程度明显减轻[(0.67±0.41)%vs(1.67±0.75)%],P62蛋白表达显著降低(0.21±0.02 vs 0.34±0.04)、LC3B蛋白表达显著升高(0.34±0.04 vs 0.24±0.04,P<0.05)。结论瘦素预处理可促进LC3B蛋白生成,降低P62蛋白表达,通过诱导心肌细胞自噬减轻MIRI。Objective To study the effect of leptin preconditioning on autophagy of cardiomyocytes in SD rats with myocardial ischemia/reperfusion injury.Methods Eighteen adult male SD rats were randomly divided into sham operation group, model group and preconditioning group(6 in each group).The animals in sham operation group underwent thoracotomy without ligation of blood vessels.The myocardial ischemia/reperfusion injury model was established by Longa occlusion for rats in model group and preconditioning group, and those in preconditioning group were preconditioned with leptin before the model was established.The myocardial infarction size was measured with TTC staining and the myocardial ischemia/reperfusion injury was assessed with HE staining.The expressions of P62 and LC3 B protein were detected by Western blot.Results The myocardial infarction size was significantly larger and the myocardial ischemia/reperfusion injury was significantly severer in model group and preconditioning group than in sham operation group(P<0.05).The expression level of P62 protein was significantly higher while that of LC3 B protein was significantly lower in model group than in sham operation group(P<0.05).The expression levels of P62 and LC3 B protein were significantly higher in preconditioning group than in sham operation group.The myocardial infarction size was significantly smaller, the myocardial ischemia/reperfusion injury was significantly milder, the expression level of P62 protein was significantly lower while that of LC3 B protein was significantly higher in preconditioning group than in model group(17.83%±1.86% vs 32.33%±2.29%,0.67%±0.41% vs 1.67%±0.75%,0.21±0.02 vs 0.34±0.04,0.34±0.04 vs 0.24±0.04,P<0.05).Conclusion Leptin preconditioning can promote the LC3 B protein production, downregulate the P62 protein expression and reduce the myocardial ischemia/reperfusion injury by inducing the autophagy of cardiomyocytes in adult SD rats.

关 键 词：瘦素 肌细胞 心脏 自噬 心肌再灌注损伤 缺血预处理 心肌 心肌梗死 

分 类 号：R542.2[医药卫生—心血管疾病]