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作 者:王春丽 孙骁 周敏 王凤丹 Wang Chunli;Sun Xiao;Zhou Min;Wang Fengdan(Department of cardiac surgery,Ninth People's Hospital of Shanghai City,Shanghai 201900,China.)
机构地区:[1]上海市第九人民医院心脏外科,上海201900
出 处:《中国循证心血管医学杂志》2021年第5期588-591,共4页Chinese Journal of Evidence-Based Cardiovascular Medicine
基 金:上海市科学技术委员会科研计划项目(19401950401)。
摘 要:目的探讨微小RNA-153-3p(miRNA-153-3p)对阿霉素性心力衰竭小鼠心肌线粒体损伤的影响。方法30只SD小鼠分为对照组、模型组、处理组,每组10只,应用阿霉素制备心力衰竭小鼠模型,并采用miRNA-153-3p antagomir干预,比较各组小鼠的心肌细胞凋亡率、线粒体功能[线粒体膜电位(MMP)、线粒体三磷酸腺苷(ATP)含量]、心肌细胞线粒体结构变化、心肌组织中miRNA-153-3p水平。结果处理组和模型组小鼠的心肌细胞凋亡率高于对照组(P<0.05);处理组小鼠的心肌细胞凋亡率低于模型组(P<0.05);处理组和模型组小鼠的心肌细胞MMP和线粒体ATP含量低于对照组(P<0.05);处理组小鼠的心肌细胞MMP和线粒体ATP含量高于模型组(P<0.05)。透射电镜观察结果显示,对照组小鼠的心肌细胞线粒体形态和结构均正常,模型组小鼠的心肌细胞线粒体结构模糊,可见脂质沉积,肌丝排列不整齐,并伴有肌丝断裂和溶解,伴有空泡变性及肌浆网腔扩张,处理组小鼠的心肌细胞线粒体结构损伤形态较模型组有明显改善。处理组和模型组小鼠心肌组织中的miRNA-153-3p水平高于对照组(P<0.05);处理组小鼠心肌组织中的miRNA-153-3p水平低于模型组(P<0.05)。结论抑制微小RNA-153-3p表达能减轻阿霉素性心力衰竭小鼠心肌细胞线粒体结构损伤,促进受损心肌细胞线粒体功能恢复。Objective To investigate the influence of microRNA-153-3p(miRNA-153-3p)on cardiomyocyte mitochondrial injury in mice with adriamycin-induced heart failure(ADR-induced AF).Methods SD mice(n=30)were divided into control group,model group and treatment group(each n=10).AF model was established by using ADR in mice,and miRNA-153-3p antagomir was used for intervention.The apoptosis rate of cardiomyocytes,mitochondrial functions[mitochondrial membrane potential(MMP),adenosine triphosphate(ATP)],changes of cardiomyocyte mitochondrial structure and level of myocardial miRNA-153-3p were compared among all groups.Results The apoptosis rate of cardiomyocytes was higher in treatment group and model group than that in control group(P<0.05),and was lower in treatment group than that in model group(P<0.05).The levels of MMP and ATP were lower in treatment group and model group than those in control group(P<0.05),and were higher in treatment group than those in model group(P<0.05).The results of transmission electron microscope observation showed that cardiomyocyte mitochondrial morphology and structure were normal in control group.In model group,the cardiomyocyte mitochondrial structure was fuzzy,lipid deposition was observed,myofilaments arranged irregular,accompanied by broken and dissolved myofilaments,vacuolar degeneration and lumen cavity expansion,and in treatment group,the injury of cardiomyocyte mitochondrial structure were significantly relieved.The level of miRNA-153-3p was higher in treatment group and model group than that in control group(P<0.05),and was lower in treatment group than those in model group(P<0.05).Conclusion The inhibition of miRNA-153-3p expression can relieve the injury of cardiomyocyte mitochondrial structure and improve the recovery of cardiomyocyte mitochondrial function.
关 键 词:微小RNA-153-3p 阿霉素 心力衰竭 心肌细胞 线粒体结构 线粒体功能 凋亡 小鼠
分 类 号:R541.61[医药卫生—心血管疾病]
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