标本配穴电针预处理对心肌缺血再灌注损伤大鼠CTGF表达的影响

Effect of the Pretreatment with Electric Acupuncture of “Combined Biao and Ben Acupoints” on CTGF in Myocardial Ischemia-reperfusion Injury

目的观察标本配穴电针预处理对心肌缺血/再灌注损伤(MI/RI)大鼠结缔组织生长因子(CTGF)表达的影响,为防治MI/RI提供新靶点新思路。方法40只雄性Wistar大鼠随机均分为假手术对照组、模型对照组、内关电针预处理组和标本配穴电针预处理组,采用鼠衣捆绑大鼠的同时,对标本配穴组和内关组进行电针治疗,第8天行心肌缺血再灌注造模,假手术对照组大鼠心脏只穿线不接扎。检测心肌CTGF、胶原容积分数(CVF)及血清标志物心肌组织活性氧(ROS)、谷胱甘肽过氧化物酶(GSH-PX)。结果与假手术组比较,模型组ROS含量、CTGF表达及CVF显著上升(P<0.05),GSH-PX活性显著下降(P<0.05);与模型组比较,标本配穴组和内关组心肌组织ROS含量、CTGF表达及CVF显著降低(P<0.05),GSH-PX活性上升(P<0.05),且标本配穴组疗效优于内关组(P<0.05)。结论标本配穴电针预处理通过调控ROS、GSH-PX的活性减轻氧化应激反应,控制CTGF的表达抑制心肌纤维化起到抗心肌缺血再灌注损伤的作用。

Objective To observe the effect of the pretreatment with electric acupuncture(EA)of"combined biao and ben acupoints"on connective tissue growth factor(CTGF)in myocardial ischemia-reperfusion injury,to provide new therapeutic target for prevention and treatment of MI/RI.Methods 40 male Wistar rats were randomly divided into model group,sham group,EA Neiguan group(PC6)and EA combined biao and ben group(ST36,RN4,PC6).Rats were bundled by rat clothing,EA Neiguan group and EA combined biao and ben group were used EA once a day.On the 8 th day,myocardial ischemia reperfusion was performed for modeling;the rats in sham group were not ligated by thoracotomy.Then test the expression of CTGF,collagen volume fraction(CVF)and the level of serum markers reaction oxygen species(ROS)in myocardial tissue,glutathione peroxidase(GSH-PX).Results Compared with sham group,the level of ROS,expression of CTGF and CVF in model group were evidently higher(P<0.05)and the activity of GSH-PX was lower in model group(P<0.05).The level of ROS,expression of CTGF and CVF in both EA combined biao and ben group and EA Neiguan group were apparently lower than model group(P<0.05),and the activity of GSH-PX was higher than model group(P<0.05).The curative effect in EA combined biao and ben group was better than EA Neiguan group(P<0.05).Conclusion The pretreatment with EA combined biao and ben could reduce oxidative stress reaction through regulating the level of serum markers and control the expression of CTGF to resist myocardial fibrosis to prevent myocardial ischemia-reperfusion injury.