【摘要】 目的探讨胸腺肽β4在大鼠心肌梗死模型中介导心脏功能保护机制。方法选择雌性SD大鼠54只,通过左前降支冠状动脉结扎建立心肌梗死模型,随机分为2组:实验组大鼠腹腔内注射胸腺肽β4(5 mg/kg),对照组大鼠腹腔内注射磷酸盐缓冲液,每组27只。2～4周后心脏超声测量大鼠心功能(左心室收缩末内径、左心室舒张末内径、左心室短轴缩短率、左心室射血分数),Western blot检测梗死区生物活性蛋白因子,并测量心肌梗死面积和心肌收缩速率。结果与对照组比较,实验组大鼠注射胸腺肽β4后,心肌缺血组织中血管生长因子相关蛋白表达明显升高,心脏功能与心肌的收缩速率明显升高,而心肌梗死面积明显缩小,差异有统计学意义(P<0.05)。结论胸腺肽β4保护心脏功能防止心肌缺血后器官功能失调。更多还原

【Abstract】 Objective To explore the mechanism of thymosinβ4-mediated cardioprotection in rat model of myocardial infarction.Methods Myocardial infarction models were created in 54 male Sprague-Dawley rats by left anterior descending coronary artery ligation.They were divided randomly into 2 groups of 27 rats each:treatment group was injected intraperitoneally with thymosin (34 and control group with PBS.Vascular growth factor-associated protein expression and cardiac functionsGeft ventricular end systolic diameter,left ventricular end diastolic diameter,left ventricular FS,left ventricular ejection fraction) were evaluated by Western blot and echcardiography after 2 and 4 weeks,respectively.Infarct size and myocardial contraction velocity were examined. Results Compared with control group,in treatment group,vascular growth factor-associated protein was significantly increased in cardiac tissue,and increase in myocardial contraction velocity and cardiac function were achieved due to thymosinβ4 therapy,while the infarct size was reduced (P<0.05).Conclusion These findings suggest that Tβ4 protect cardiac tissue against post-is-chemic organ dysfunction.更多还原