PI3K/Akt信号通路介导芪丹通脉片抑制缺血再灌注大鼠心肌细胞凋亡  

Anti apoptotic effect of Qidan Tongmai tablet in myocardium ischemia-reperfusion injury mediated by PI3K/Akt signaling pathway

作　　者：李军昌 王宗仁 李秋霞[2] 张海峰[3] 王文 王跃民[3] 李晶华 

机构地区：[1]第四军医大学第一附属医院中医科,陕西西安710032 [2]陕西师范大学运动生物学研究所,陕西西安710062 [3]第四军医大学基础部生理教研室,陕西西安710032

出　　处：《中国现代医学杂志》2007年第10期1183-1186,共4页China Journal of Modern Medicine

基　　金：陕西省中医管理局(2005074)

摘　　要：目的观察芪丹通脉片对缺血再灌注(MI/R)大鼠心肌细胞凋亡的影响及其与PI3K/Akt信号通路活化的关系。方法雄性SD大鼠随机分为4组:(A)假手术组;(B)缺血再灌注组;(C)芪丹通脉片预处理+缺血再灌注组;(D)芪丹通脉片处理组+缺血再灌注+LY294002。大鼠麻醉开胸,结扎冠状动脉前降支40min,再灌注4h。TUNEL方法定性和定量检测心肌细胞凋亡;Westernblot测定信号蛋白的表达。结果芪丹通脉片能够抑制心肌细胞的凋亡[(20.3±4.5)%vs(11.6±2.3)%,P<0.01];并能够增加Akt的磷酸化水平,而这种抗凋亡作用能够被磷脂酰肌醇3激酶(phosphatidyl inositol 3 kinasePI3K)/丝氨酸苏氨酸蛋白激酶(serine/threonine kinase,Akt)信号通路阻断剂LY294002所抑制。结论芪丹通脉片能够抑制缺血再灌注所致的心肌细胞凋亡,这种保护作用与生存信号通路PI3K/Akt的活化所介导。[Objective] To investigate the signaling pathway involved in the inhibition of apoptotic effect during myocardium ischemia reperfusion with Qidan Tongmai tablet, [Methods] Male SD rats were divided randomly into four groups. Male Sprague-Dawley rats were anesthetized and open-chest animals were subject to 40 min of mycardial isehemia followed by 4h-reperfusion. Cardiac myocyte apoptosis was determined both qualitatively and quantitatively by terminal deoxynucleotidyl transfease-mediated dUTP nick-end labeling （TUNEL） methods. The state of PI3K signaling cascade was determined by Westembloting analysis. [Result] Apoptosis index （AI） was attenuated from （20.3±4.5）% in control vs （11.6±2.3）% in QDTMT-treated animals. The state of p-Akt was induced a 2.5 fold increase by QDTMT administration. LY294002 abrogated the anti apoptosis effect. [（17.0±5.5）% vs （20.3±4.5）%]. [ Conclusion ] the results suggest that QDTMT may be able to inhibit the myoeyte apoptosis against reperfusion-induced injury mediated by the increase of phosphorylating Akt.

关 键 词：芪丹通脉片 益气活血法 再灌注损伤 心肌 PI3K/AKT 

分 类 号：R285.5[医药卫生—中药学]