促红细胞生成素B螺旋结构缩氨酸对大鼠心肌缺血损伤的影响

The cardioprotective effect of a small nonerythropoietic helix B surface peptide based upon erythropoietin structure on heart ischemic myocardial damage in rat

目的探讨促红细胞生成素(rhEPO)B螺旋结构缩氨酸(pHBP)对大鼠心肌缺血损伤的影响及其机制。方法采用结扎冠状动脉前降支的方法建立大鼠急性心肌梗死(AMI)模型。90只大鼠随机分为四组:假手术组(A组,n=10)、AMI组(C组,n=20)、rhEPO组(G组,n=30)和pHBP组(E组,n=30)。建模后注射rhEPO、pHBP,24h后通过TCC染色测量MI面积。术后3、24h,Western blot法检测信号转导子与转录激活子3(STAT3)蛋白表达。8周后,通过超声心动图测量左心室舒张期末容积(LVEDV)、左心室收缩期末容积(LVESV)和左心室射血分数(EF)。结果与C组比较,E、G组MI面积明显减小(P<0.05)。与A组比较,E、G组STAT3蛋白表达明显增高(P<0.05)。与A组比较,E组和G组LVEDV和LVESV明显升高,EF明显降低(P<0.01)。与C组比较,E组和G组LVEDV和LVESV明显降低,EF明显升高(P<0.05)。结论 pHBP在大鼠心肌缺血损伤中具有心脏保护作用,其保护机制可能与其抑制心肌细胞凋亡和促进新生血管形成有关。

Objective To investigate the protective effects of a small nonerythropoietic helix B surface peptide based upon erythropoietin structure on heart ischemic myocardial damage in the rat.Methods Rat models of AMI which were built by ligating the left anterior descending coronary artery.Ninty rats were randomly divided into sham-operated group（group A,n=10）,control group （group C,n=20）,rhEPO group（group G,n=30） and pHBP treatment group（group E,n=30）.After establiblishment of experiment of model,rats were given an injection of rhEPO,pHBP,the myocardial infarction area was evaluated by TCC dyeing after 24 hours; After 3 hours,24 hours of treatment,the expression of STAT3 was analysized through by Western blot; we assessed the LV end-diastolic volume （EDV）,LV end-systolic volume（ESV）,LV ejection fraction（EF％） of the rat by echocardiography after 8 weeks.Results The myocardial infarct size of the group G and E was decreased significantly than group C（P＜0.05）.Compared with group A,the expression of STAT3 was increased significantly in group E and G（P＜0.05）.Compared with group A,the LVEDV and LVESV were increased obviously,the EF was decreased significantly in group E and G （P＜0.05）.Compared with group C,the LVEDV and LVESV were decreased and the EF was increased significantly in group E and G （P＜0.05）.Conclusion pHBP has a cadioprotective effect on heart ischemic damage.The protective mechanism may be related to the function of inhibition of myocardial cell apoptosis and inducing neovascularisation.