妊娠期缺氧对子代大鼠脑皮质肾素-血管紧张素系统的影响  

Effect of prenatal hypoxia on the expression of local renin-angiotensin system in cerebral cortex from rat offspring

作　　者：李美美[1] 黄子扬[1] 王凌星[1] 王振华[1] 

机构地区：[1]福建医科大学附属第二临床医院心内科,泉州362000

出　　处：《福建医药杂志》2014年第2期67-69,共3页Fujian Medical Journal

摘　　要：目的探讨妊娠期慢性缺氧对子代大鼠脑皮质血管紧张素转换酶(ACE)及血管紧张素Ⅱ受体1、2(AT1R、AT2R)表达的影响。方法建立SD雌鼠妊娠期缺氧模型。采用RT-PCR、Western blot法检测子代大鼠大脑皮质ACE mRNA表达以及AT1R、AT2R蛋白表达。结果缺氧组子代大鼠大脑皮质ACE mRNA表达比对照组增强(P<0.05),AT1R蛋白表达比对照组减少(P<0.05),而AT2R蛋白表达却增多(P<0.05),以上改变随年龄增长仍持续性存在。结论妊娠期缺氧可增强子代大鼠成年后大脑皮质ACE及AT2R表达并抑制AT1R表达,这可能与妊娠期缺氧引起子代大鼠脑皮质神经元变性、凋亡有关。Objective To study the effect of chronic hypoxia during pregnancy on the expression of ACE and the recep- tors of Ang II （AT1R, AT2R） in cerebral cortex of rat offspring. Methods Maternal hypoxic model was established in Sprague Dawley rats. The expressions of ACE at the mRNA level was detected by RT-PCR and the expression of the receptors of Ang II （ATIR, AT2 R） were determined at the protein level by Western blot in the offspring. Results The mRNA expression of ACE in cerebral cortex increased significantly in the offspring of hypoxic exposure group compared to the controls （P〈0.05）, while the level of AT1 R protein decreased significantly and AT2 R protein increased significantly in the offspring of hypoxic exposure group. The above changes still continued as the age increased. Conclusion Prenatal hypoxia enhances the expression of ACE and AT2 R, and inhibits that of AT1 R in cerebral cortex of the offspring. That might be associated with neuronal degeneration or apoptosis in cerebral cortex.

关 键 词：妊娠期缺氧 大脑皮质 脑皮质血管紧张素转换酶 血管紧张素Ⅱ受体1 血管紧张素Ⅱ受体2 

分 类 号：R714.25[医药卫生—妇产科学]