【作者】 封芬；

【导师】 陈临溪；

【作者基本信息】 南华大学 ， 药理学， 2007， 硕士

【摘要】 目的:研究apelin-APJ系统在心肌肥厚形成中的意义,并初步探讨apelin-APJ参与心肌肥厚过程的caveolin-1-PI3K-Akt-p70S6K及caveolin-1-ERK1/2信号通路的分子机制。方法:用腹主动脉环扎缩窄术建立左室肥厚(LVH)的SD大鼠动物模型。用western blot检测大鼠心肌组织和大鼠胚胎心肌细胞株H9c2细胞的ACE2、APJ、caveolin-1和PI3K、pAkt、p-p70S6k、ERK1/2、pERK1/2的表达。结果: 1、与假手术组比较,左室肥厚大鼠模型的肥厚心肌中APJ表达增加,caveolin-1、ACE2表达减少,ERK1/2、pERK1/2、PI3K、pAkt、p-p70S6k表达增加;2、apelin (2μM,4h)刺激培养的心肌细胞系H9c2细胞引起caveolin-1表达减少,PI3K、pAkt、p-p70S6k、pERK1/2表达增加,APJ、ERK1/2表达没有明显变化。结论:1.Apelin-APJ与大鼠心肌肥厚形成有关。2 . Apelin-APJ参与大鼠心肌肥厚发生可能与caveolin-1-PI3K-Akt-p70S6k及caveolin-1-ERK1/2信号通路有关。更多还原

【Abstract】 AIM: To investigate of apelin/APJ involved in the process of rat myocardial hypertrophy and the signal pathway of caveolin-1-PI3K-Akt-p70S6k and caveolin-1- ERK1/2 stimulated by apelin-13 in H9c2 cardiocyte cells.Methods: The left ventricular hypertrophy rats model was established following coarctation of abdominal aorta. The expression of ACE2, APJ, caveolin-1, PI3K, pAkt, p-p70S6k, ERK1/2 and pERK1/2 were observed by Western Blot in heart tissue and H9c2 cells.Results: At animal experiment,western blotting analysis showed that the expression of APJ, caveolin-1 and ACE2 decreased, and the expression of ERK1/2, pERK1/2, PI3K, pAkt and p-p70S6k increased. At cell experiment, similarly, apelin-13 promoted the expression of PI3K, pAkt, pERK1/2, p-p70S6k and decreased the expression of caveolin-1.Conclusion: Apelin/APJ expression increased in the process of myocardial hypertrophy, and the effects maybe involved in apelin/APJ-caveolin-1-PI3K-Akt-p7oS6k and apelin/APJ-caveolin-1-ERk1/2 signal cascades.更多还原