第四军医大学学报2009,Vol.30Issue(22) :2587-2590.

PI3K/Akt信号通路对血管内皮功能的影响及促红素干预

Effects of PD K/Akt signaling pathway on vascular endothelial function and interventional effects of erythropoietin

邱清艳 秦俭 郑维平 高电萨 赵倩
第四军医大学学报2009,Vol.30Issue(22) :2587-2590.

PI3K/Akt信号通路对血管内皮功能的影响及促红素干预

Effects of PD K/Akt signaling pathway on vascular endothelial function and interventional effects of erythropoietin

邱清艳 1秦俭 1郑维平 1高电萨 1赵倩1
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作者信息

  • 1. 重庆医科大学附属第一医院心血管内科,重庆,400016
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摘要

目的:研究P13K/Akt信号通路对心肌缺血后处理(I-PostC)大鼠血管内皮功能的影响及重组人促红细胞生成素注射液(rhEPO)的干预.方法:42只SD雄性大鼠随机分为7组:假手术组(Sham组),缺血/再灌注(I/R)组(IfR组),缺血后处理组(I-PostC组),渥漫青霉素+I-PostC组(Wort+I-PostC组),重组促红细胞生成素组(rhEPO组),Wort+rhEPO组,rhEPO+I-PostC组.结扎大鼠冠状动脉左前降支建立I/R模型.RT-PCT检测各组主动脉组织中Akt mRNA水平,取胸主动脉制成条片行离体器官灌流实验,测定其对去氧肾上腺素(PE)的收缩反应、对乙酰胆碱(Ach)的内皮依赖性舒张反应和对硝普钠(SNP)的非内皮依赖性舒张反应.结果:经I-PcostC和rhEPO的于预后,均能改善各组大鼠I/R损伤的血管内皮对乙酰胆碱的舒张反应,增加主动脉组织中Akt mRNA的表达,但两者的上述效应差异无统计学意义;PI3K阻滞剂Wort可削弱两者的上述效应;联合应用I-PcostC,rhEPO与两者单独应用相比较差异不显著.结论:I-PostC,rhEPO干预,可通过激活P13K-Akt信号通路发挥血管内皮保护作用.

Abstract

AIM: To investigate the effects of PI3K/Akt signaling pathway on vascular endothelial function in rats with myocardial ischemic postconditioning(I-PostC) and interventional effects of erythropoietin. METHODS: Forty-two male SD rats were randomized into 7 groups: Sham operation group( Sham group) ,ischemia/reperfusion group ( I/R group ), Ischemia-Postconditioning group( I-PostC group) , Wortmannin + I-Post group( Wort + I-PostC group) , rherythropoietin group ( rhEPO group) , Wort + rhEPO group and rhEPO + I-Postc group. Rat models with I/R were induced by ligation of the coronary artery in SD rats. RT-PCR was used to determine Akt mRNA level in each group. Thoracic aortas were harvested and were cut into strips for isolated perfusion experiment on contraction to phenylephrine( PE), endothelium-dependent diastole to acetylcholine(Ach) and non-endothelium-dependent diastole to sodium nitroprusside(SNP). RESULTS: The intervention of I-PcostC and rhEPO could improve strips of thoracic aortas's dilatant reaction to acetylcholine after ischemia/reperfusion injury and increase the expression of Akt mRNA level in the aortas. There's no significant statistical difference in effects of the two methods above. Wort, the inhibitor of PI3K,eould impair the effects; Combined use of I-PcostC and rhEPO showed no statistical difference compared with only use I-PcostC or rhEPO. CONCLUSION: I-PostC and rhEPO can play a role in protecting vascular endothelial function via PI3K/Akt signal transduction pathway.

关键词

缺血/再灌注/缺血后处理/rhEPO/内皮功能/PI3K/Akt信号通路

Key words

ischemia/reperfusion/ischemic-postconditioning/rhE-PO/endothelial function/PI3K/Akt signaling pathway

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出版年

2009
第四军医大学学报
第四军医大学

第四军医大学学报

CSTPCDCSCD北大核心
影响因子:0.599
ISSN:1000-2790
被引量3
参考文献量10
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