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目的:探讨甲状腺素致心肌细胞肥大的相关机制。方法:取分离培养的乳鼠心肌细胞,用L-甲状腺素(T3)诱导心肌细胞肥大,然后再加入磷脂酰肌醇-3-激酶(PI3-K)抑制剂LY294002和哺乳动物雷帕霉素靶蛋白(mTOR)特异性抑制剂雷帕霉素进行干预;采用测量心肌细胞表面积及3H-亮氨酸掺入、Western blot等检测方法。结果:甲状腺素诱导的心肌细胞肥大能被LY294002或雷帕霉素抑制,LY294002能抑制甲状腺素激活丝氨酸/苏氨酸激酶(AKT)和mTOR,雷帕霉素能特异性阻断mTOR的活化。结论:甲状腺素能通过PI3-K/Akt-mTOR信号通路促进心肌细胞肥大。
Objective: To investigate the mechanism of thyroid hormone-induced hypertrophy in cardiomyocytes. Methods: Cardiomyocytes were isolated from neonatal rat hearts and cardiomyocytes were induced to hypertrophy by L-thyroxine (T3) and then added with phosphatidylinositol 3-kinase (PI3-K) inhibitor LY294002 and mammalian rapamycin The specific inhibitor of target protein (mTOR) rapamycin intervention; measurement of myocardial cell surface area and 3H-leucine incorporation, Western blot and other detection methods. RESULTS: Thyroxine-induced cardiomyocyte hypertrophy could be inhibited by LY294002 or rapamycin. LY294002 inhibited thyroxine-activated serine / threonine kinase (AKT) and mTOR, and rapamycin specifically blocked the activation of mTOR. Conclusion: Thyroxine can promote cardiomyocyte hypertrophy through the PI3-K / Akt-mTOR signaling pathway.