脂联素通过增强线粒体生物合成和功能减轻高糖/高脂诱导的心肌细胞损伤

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500 μmol/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，500 μmol/L软脂酸钠和3 μg/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。

Adiponectin exerts cardioprotective effects against high-glucose/high-fat-induced injury of neonatal rat cardiomyocytes through increasing mitochondrial biogenesis and function

AIM:To investigate whether adiponectin (APN) generates cardioprotection in response to high-glucose/high-fat damage through increasing mitochondrial biogenesis and functions. METHODS: Cultured neonatal rat ventricular myocytes (NRVM) were randomized into control group (5 mmol/L glucose and 20 mmol/L mannitol), high-glucose/high-fat group (25 mmol/L glucose and 500 μmol/L sodium palmitate, 18 h incubation) and high-glucose/high-fat+APN group (25 mmol/L glucose, 500 μmol/L sodium palmitate and 3 μg/ml globular APN, 18 h incubation) after 3 days of normal culture. Cells were harvested for evaluation of mitochondrial membrane potential and mRNA levels of Tfam after high-glucose/high-fat incubation. RESULTS: Compared with those in control group, both mitochondrial membrane potential and mRNA levels of Tfam decreased and cell apoptosis increased in high-glucose/high-fat group. However, these changes were reversed by APN. CONCLUSION: High-glucose/high-fat can lead to mitochondrial dysfunction in cardiomyocytes and APN can protect cardiomyocytes by increasing mitochondrial biogenesis and functions.