与细胞骨架同源10号染色体有缺陷的磷酸酯酶和磷脂酰肌醇-3激酶在大鼠心肌肥厚中的表达

Expression of phosphatase and tensin homology deleted on chromosome ten and phosphaditylinositol 3-kinase in rat cardiac hypertrophy

目的：研究异丙肾上腺素致大鼠心肌肥厚与细胞骨架同源10号染色体有缺陷的磷酸酯酶（PTEN）和磷脂酰肌醇-3激酶（P13K）在心肌组织中的表达，为探讨心肌肥厚的信号转导机制和逆转心肌肥厚提供形态学资料。方法：健康成年SD大鼠皮下注射异丙肾上腺素，造成心肌肥厚模型；取心肌组织，常规石蜡切片，H—E染色，观察心肌组织的病理变化；免疫组织化学显色和免疫荧光显色，检测PTEN和p-P13K的表达及分布。利用图像分析软件对PTEN和p-P13K的表达结果进行定量分析。结果：与对照组相比，实验组PTEN和p-P13K的阳性表达增高。结论：PTEN和p-P13K蛋白表达增高可能在心肌肥厚的发生和发展过程中发挥重要作用。

Objective： To provide morphological data for the investigation of the cardiac hypertrophy signal transduction mechanism and reversal of cardiac hypertrophy by studing the expression of PTEN and PI3K in cardiac tissue in isoproterenol-induced myocardial hypertrophy. Methods： Cardiac hypertrophy models were established by subcutaneous injection of isoproterenol into healthy adult SD rats. The pathological changes of myocardial tissues were observed by conventional paraffin section and H-E staining. The expression and distribution of PTEN and p-PI3K was detected by immunohistochemistry and immunofluorescenee staining. Image analysis software was used to conduct quantitative analysis. Results： Compared with the control group, the positive expression of PTEN and p-PI3K in the experimental group was significantly increased. Conclusion： The increase of PTEN and p-PI3K protein expression may play an important role in the occurrence and development of cardiac hypertrophy.