中文摘要：

目的探讨SonicHedgehog信号通路在正常心脏和缺血缺氧的心肌细胞的激活与表达.方法用左前降支结扎法构建心肌梗死模型,并用超声心动图鉴定.采用Westernblot和免疫荧光染色分别检测12例心肌梗死组织,9例正常心肌组织,H9C2及H2O2 诱导下的H9C2细胞的Shh、Ptch-1、Smo、Gli-1的表达.注射激动剂及抑制剂于H2O2 诱导的缺血缺氧H9C2的细胞模型,再次检测Shh、Ptch-1、Smo、Gli-1的表达及强弱.结果Shh、Gli-1在心肌梗死心脏表达,Ptch-1、Smo在正常心脏及心肌梗死心脏均表达,缺血缺氧H9C2细胞模型的Shh、Gli-1表达增加.H2O2 诱导下的H9C2表达Gli-1、Shh,Ptch-1、Smo在正常H9C2和H2O2诱导下的H9C2均有表达.结论Shh信号通路在缺血与氧化应激条件下被激活,并且具有促进心肌细胞的损伤修复作用.

英文摘要：

Aim To investigate the effect of Sonic Hedgehog on normal hearts and hypoxic-ischemic myo-cardial cells. Methods A method for left anterior de-scending artery ( LAD ) ligation was employed to con-struct the myocardial infarction model, and ultrasonic cardiogram was used for identification. Western blot and immunofluorescence staining were used to detect expressions of Shh, Ptch-1, Smo and Gli-1 in H9C2 cells and H2 O2-induced H9C2 cells, and that in 12 ca-ses of myocardial infarction tissues and 9 cases of nor-mal myocardium, respectively. Agonist and antagonist of Shh pathway were adminstered in the hypoxic-ische-mic myocardial H2 O2-induced H9C2 cell model, and once again expressions and strength of Shh, Ptch-1, Smo, Gli-1 were detected. Results Shh and Gli-1 were not expressed in normal hearts, but expressed in hearts with myocardial infarction;Ptch-1 and Smo were expressed in both normal hearts and hearts with myo-cardial infarction. Under the action of agonist, expres-sions of Shh and Gli-1 increased in the hypoxic-ische-mic H9C2 cell model. Similarly, Shh and Gli-1 were not expressed in normal H9C2 cells, but in H2 O2-in-duced H9C2 cells, and Ptch-1 and Smo were expressed in both normal H9C2 and in H2 O2-induced H9C2 cells. Conclusion Shh signaling pathway can be acti-vated in the condition of ischemia and oxidative stress, and then it promotes the repairing of myocardial cell damage.