摘要
目的：观察PTEN/PI3K信号通路在大鼠心肌组织中的表达,探讨该通路在心肌肥厚发生、发展中的作用.方法：皮下注射异丙肾上腺素（ISO）建立大鼠心肌肥厚模型,测定大鼠体质量、心质量、心肌细胞横径和横截面积;采用免疫组织化学方法检测大鼠心肌组织中肥大标志因子β-肌球蛋白（β-MHC）及PTEN/PI3K信号通路上PTEN、磷脂酰肌醇3激酶（PI3K）、蛋白激酶B（PKB）、死亡相关因子（BAD）蛋白表达;利用计算机图像处理系统对各种蛋白进行定量分析.结果：模型组大鼠全心质量/体质量、左室质量/体质量、心肌细胞横径、心肌细胞截面积较对照组明显增加.模型组大鼠的心肌组织与对照组相比,β-MHC、PI3K与PKB表达水平均升高,PTEN和BAD表达水平明显降低.结论：PTEN在心肌肥厚中表达明显降低,起负性调节作用;PI3K/PKB信号通路激活,可能是导致心肌肥厚的机制之一,BAD可望成为生物学治疗靶点.
Objective： To investigate the expression of phosphatase and tensin homologue deleted on chromosome ten （PTEN）/phosphatidylinositol 3 kinase （PI3K） signal pathways in hypertrophic myocardium of rats and the effect of this pathway in process of cardiac hypertrophy. Methods： Through the rat models of cardiac hypertrophy by low dose isoproteronol （ISO）, cardiac hypertrophy indexes （heart mass, left ventricular mass, body mass） were calculated; the expressions of β-myosin heavy chain （β-MHC）, PTEN, PI3K, protein kinase B （PKB） and Bcl-XL/Bcl-2-associated death promoter （BAD） were detected by immunohistoehemistry. Results： The radio of heart weight/body weight and the radio of left ventricular weight/body weight, transdiameter of cardiocyte, cardiocyte area and cardiac level of β-MHC expression were increased markedly in ISO group compared with those in the control group. Compared with the degree of the hypertrophy, PI3K and PKB expressions were increased, and PTEN and BAD expressions were decreased. Conclusion： PTEN expression is decreased in cardiac hypertrophy and PTEN is an important endogenous inhibitor of cardiac hypertrophy. PI3K/PKB pathways are inviolved in the signal transduction of cardiac hypertrophy in rat, and BAD might be a new target in biology therapy.
出处
《解剖学杂志》
CAS
CSCD
北大核心
2010年第2期172-175,共4页
Chinese Journal of Anatomy
基金
河南省科技厅立项课题（072300450300）
