Akt信号通路在紫绀型先天性心脏病患儿心肌慢性缺氧适应中的作用  

Role of Akt signal pathway in chronically hypoxic children with cyanotic congenital heart disease

作　　者：谢婧雯[1] 刘晓燕[1] 

机构地区：[1]重庆医科大学附属儿童医院心内科儿童发育疾病研究省部共建教育部重点研究室儿科学重庆市重点实验室重庆市(儿童发育重大疾病诊治与预防)国际科技合作基地,重庆400014

出　　处：《临床心血管病杂志》2012年第5期373-376,共4页Journal of Clinical Cardiology

基　　金：重庆市教委科研项目(No:kj100321)

摘　　要：目的:探讨Akt信号通路在紫绀型先天性心脏病患儿心肌慢性缺氧适应中的意义。方法:收集紫绀型和非紫绀型先天性心脏病患儿共50例,其中紫绀型26例(紫绀组),动脉血氧饱和度(SaO2)60%～89%;非紫绀型24例(非紫绀组),SaO2>95%,均不伴肺动脉高压[肺动脉收缩压<30mmHg(1mmHg=0.133kPa)]。心脏外科手术体外循环前留取右心耳组织,应用Western blot方法检测心肌组织蛋白激酶B(总Akt)和磷酸化蛋白激酶B(Ser473P-Akt)表达水平,免疫组织化学技术检测心肌组织总Akt和Ser473 P-Akt蛋白表达部位与水平。结果:与非紫绀组相比,紫绀组患儿心肌组织Ser473P-Akt蛋白表达水平明显增高(P<0.01),而2组患儿总Akt蛋白表达水平差异无统计学意义(P>0.05)。紫绀组患儿心肌组织Ser473P-Akt蛋白大部分表达在心肌细胞的胞质,胞核亦有微弱表达,而非紫绀组心肌细胞则无明显Ser473P-Akt蛋白表达。2组患儿总Akt蛋白绝大部分也表达在心肌细胞的胞质,胞核亦有微弱表达,但表达部位和水平差异无统计学意义。紫绀组患儿心肌组织Ser473 P-Akt蛋白表达水平与患儿术前SaO2呈负相关(r=-0.771,P<0.01)。结论:Akt信号通路激活可能是紫绀型先天性心脏病患儿心肌慢性缺氧适应的重要信号调控机制之一。Objective：To explore the effect of Akt signal pathway in chronically hypoxic children with cyanotic congenital heart disease（CHD）.Method：When the cardiopulmonary bypass was not established before cardiac surgery,samples from the auricle of right atrium were collected from children who were not associated with pulmonary arterial hypertension with cyanotic（n=26,SaO2： 60%-89%） and acyanotic（n=24,SaO2〉95%） CHD.The level and site of the protein expression of Akt and Ser473P-Akt were examined by Western blot and immunohistochemistry.Result：There was no statistical difference between cyanotic and acyanotic groups in Akt protein expression（P〈0.05）,however,the protein level of Ser473P-Akt in cyanotic group was significantly higher than that in acyanotic group（P〈0.01） and was negatively correlated with preoperative SaO2.Conclusion：Cyanotic hearts adapt to chronic hypoxia through activation of Akt signal pathway,which is responsible for cardioprotection in the chronically hypoxic children with cyanotic CHD.

关 键 词：先天性心脏病 慢性缺氧 蛋白激酶B(Akt) 磷酸化蛋白激酶B 

分 类 号：R541.1[医药卫生—心血管疾病]