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目的:观察脂联素(APN)是否通过增强线粒体生物合成和功能减轻高糖/高脂所致心肌细胞损伤。方法:分离培养SD乳鼠的心肌细胞,培养3 d后分为3组:即对照组(培养基中含5 mmol/L葡萄糖和20 mmol/L甘露醇)、高糖/高脂组(培养基中含25 mmol/L葡萄糖和500μmol/L软脂酸钠,培养18 h)及高糖/高脂+APN组(培养基中含25 mmol/L葡萄糖,500μmol/L软脂酸钠和3μg/ml APN球状片段,培养18 h)。高糖/高脂处理后,检测转录因子Tfam mRNA的水平、细胞线粒体膜电位与心肌细胞的凋亡。结果:与对照组比较,高糖/高脂组Tfam mRNA的水平与线粒体膜电位均降低,细胞凋亡增加;APN处理可逆转上述作用。结论:高糖/高脂降低心肌线粒体生物合成和导致线粒体功能障碍;APN可通过增加线粒体的生物合成和功能而发挥对心肌保护的作用。
AIM: To observe whether adiponectin (APN) attenuates cardiomyocyte injury induced by high glucose / high fat by enhancing mitochondrial biosynthesis and function. Methods: Cardiomyocytes from neonatal SD rats were isolated and cultured for 3 days. The cells were divided into 3 groups: control group (5 mmol / L glucose and 20 mmol / L mannitol), high glucose / (25 mmol / L glucose, 500 μmol / L sodium palmitate and 3 μg / ml) in medium containing 25 mmol / L glucose and 500 μmol / L sodium palmitate for 18 h and high glucose / / ml APN globular fragment, cultured for 18 h). After high glucose / high fat treatment, the levels of Tfam mRNA, mitochondrial membrane potential and cardiomyocyte apoptosis were detected. Results: Compared with the control group, the levels of Tfam mRNA and mitochondrial membrane potential were decreased and the cell apoptosis increased in the high glucose / hyperlipidemic group. APN treatment could reverse the above effects. CONCLUSION: High glucose / high fat can reduce myocardial mitochondrial biosynthesis and lead to mitochondrial dysfunction. APN can exert protective effect on myocardium by increasing mitochondrial biosynthesis and function.