PI3K/Akt信号参与介导虎杖甙对缺血/再灌注心肌的保护作用  

PI3K/Akt signaling mediates protection effects of polydatin on myocardial ischemia/reperfusion injury

作　　者：余福林 高延 王利 王海强 YU Fu-lin;GAO Yan;WANG Li;WANG Hai-qiang(Department of Cardiology,Air Force 986 Hospital,Xi’an 710054,Shaanxi,China;Department of Cardiology,Xi’an Union Hospital,Xi’an 710010,Shaanxi,China;Department of Cardiology,Xi’an Third Hospital,Xi’an 710082,Shaanxi,China)

机构地区：[1]空军第986医院心内科,陕西西安710054 [2]西安工会医院心内科,陕西西安710010 [3]西安市第三医院心内科,陕西西安710082

出　　处：《心脏杂志》2022年第4期373-377,388,共6页Chinese Heart Journal

摘　　要：目的探讨虎杖甙对小鼠心肌缺血/再灌注损伤的影响及可能机制。方法建立小鼠缺血/再灌注损伤模型,随机将小鼠分为5组(每组18只):假手术组(Sham)、缺血/再灌注组(I/R)、缺血/再灌注+虎杖甙组(I/R+PD)、缺血/再灌注+虎杖甙+LY294002组(I/R+PD+LY294002)和缺血/再灌注+LY294002组(I/R+LY294002)。小鼠心脏超声检测心功能;Masson染色评估胶原容积分数(CVF);TTC染色测定小鼠心肌梗死面积;ELISA法检测血浆CK和LDH水平;Tunel法测定小鼠心肌细胞凋亡,Western blot检测p-Akt的表达。结果与Sham组相比,I/R组LVEF和LVFS值均显著降低(P<0.05),心肌梗死面积、血浆CK和LDH水平均显著增加(P<0.05),心肌细胞凋亡显著增加(P<0.05),心肌CVF值显著增加(P<0.05),心肌p-Akt蛋白表达显著增加(P<0.05);与I/R组相比,I/R+PD组LVEF和LVFS值均显著增加(P<0.05),心肌梗死面积、血浆CK和LDH水平均显著降低(P<0.05),心肌细胞凋亡显著减少(P<0.05),心肌CVF值显著降低(P<0.05),心肌p-Akt蛋白表达进一步增加(P<0.05);与I/R+PD组相比,I/R+PD+LY294002组LVEF和LVFS值均显著降低(P<0.05),心肌梗死面积、血浆CK和LDH水平均显著增加(P<0.05),心肌细胞凋亡显著增加(P<0.05),心肌CVF值显著增加(P<0.05),心肌p-Akt蛋白表达显著减少(P<0.05)。结论虎杖甙通过激活PI3K/Akt信号通路减轻心肌I/R损伤。AIM To explore the effects of polydatin(PD)preconditioning on myocardial ischemia/reperfusion(I/R)injury.METHODS Myocardial I/R injury was produced in mice via 30 min of left descending coronary artery occlusion,followed by 24 h reperfusion.Male C57/BL6J mice were randomly divided into five groups(n=18):Sham group,I/R group,I/R+PD group,I/R+PD+LY294002 group and I/R+LY294002 group.Echocardiography was employed to evaluate the cardiac functions.The area of myocardial infarction was determined by TTC staining and the levels of plasma CK and LDH were measured by ELISA.The fibrosis degree was detected by Masson staining,cardiac apoptosis was evaluated by the Tunnel assay and the expressions of p-Akt and Akt were determined by Western blot.RESULTS Compared with those in sham group,the cardiac functions were decreased significantly(P<0.05),with enhanced CVF and apoptosis index(P<0.05)and increased levels of plasma CK and LDH(P<0.05),as well as enhanced infarct size,and the expressions of p-Akt were increased(P<0.05)in I/R group.Compared with those in I/R group,the cardiac functions were improved significantly(P<0.05),with decreased CVF and apoptosis index(P<0.05)and decreased levels of plasma CK and LDH(P<0.05),as well as decreased infarct size,and the expressions of p-Akt were further increased(P<0.05)in I/R+PD group.Compared with those in I/R+PD group,the cardiac functions were decreased(P<0.05),with enhanced CVF and apoptosis index(P<0.05)and increased levels of plasma CK and LDH(P<0.05),as well as enhanced infarct size,and the level of p-Akt was decreased(P<0.05)in I/R+PD+LY294002 group.CONCLUSION polydatin attenuates myocardial I/R injury by activating PI3K/Akt signaling.

关 键 词：虎杖甙 缺血/再灌注 磷脂酰肌醇-3激酶 蛋白激酶B 

分 类 号：R285.5[医药卫生—中药学]