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作 者:王瀚[1] 闫文俊[1] 周芬[1] 张立剑[1] 李文婷[1] 刘佩林[1] 陶凌[1]
机构地区:[1]第四军医大学西京医院心内科,陕西西安710032
出 处:《心脏杂志》2013年第2期146-150,共5页Chinese Heart Journal
基 金:国家自然科学基金项目资助(81170186;81225001)
摘 要: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 high -glucose/high-fat investigate whether adiponectin (APN) damage through increasing mitochondrial generates cardioprotection in response to biogenesis and functions. METHODS: Cultured neonatal rat ventricular myocytes (NRVM) were randomized into control group (5 mmol/L glu- cose and 20 mmol/L mannitol) , high-glucose/high-fat group (25 mmol/L glucose and 500 μmol/L sodi- um 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. Ceils 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 Tram 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 increas- ing mitochondrial biogenesis and functions.
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