针灸预处理对大鼠心肌缺血再灌注后内质网应激的影响

目的探讨针灸预处理对大鼠心肌缺血再灌注（I／R）损伤后内质网应激的影响。方法将60只大鼠分成假手术组、模型组及干预组,每组各20只。假手术组大鼠只在冠状动脉左室支左心耳下缘约0．5 cm处穿线,不结扎;模型组人鼠建立心肌I／R模型;干预组大鼠在I／R建模前7 d连续给予电针预处理。于再灌注24 h后采用TUNEL法计算心肌细胞凋亡指数（AI）、Western blots检测心肌葡萄糖调节蛋白78（GRP78）、CCAAT／增强子结合蛋白同源蛋白（CHOP）、半胱氨酸天冬氨酸蛋白酶12（caspase 12）蛋白表达,同时每组各选取5只大鼠处死取心肌以检测p38信号通路磷酸化的情况。 结果三组间AI、心肌组织GRP78、CHOP、caspase 12蛋白表达及心肌组织p38磷酸化水平比较,差异均具有统计学意义（F=8．15、12．28、20．81、18．63、36．08,P均〈0．05）,进一步两两比较,各指标模型组及干预组蛋白表达显著高于假手术组,且模型组表达更为显著（P均〈0．05）。 结论针灸予币处理可能通过抑制内质网应激对心肌T／R损伤起到保护作用,其机制可能与调节p38信号通路磷酸化水平有关。

Effects of electroacupuncture pretreatment on endoplasmic reticulum stress after myocardial ischemia reperfusion injury in rats

Objective To investigate the effects of electroacupuncture pretreatment on endoplasmic reticulum stress after myocardial ischemia reperfusion （I/R） injury in rats. Methods A total of 60 rats were randomly divided into three groups： sham-operation group, model group and treatment group, 20 rats in each group. The rats in the sham-operation group were only threaded about 0.5 cm of left lower limb at left ventricle coronary artery, the rats in the model group and treatment group all established I / R models, and the treatment group received electroacupuncture pretreatment for 7 days before the model building. The apoptotic index was recorded by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling （TUNEL）, the glucose regulated protein 78 （GRP78）, CCAAT / enhancer-binding protein homologous protein （CHOP） and caspase 12 were detected by Western blots. Meanwhile, the myocardial p38 lightning phosphorylation sacrificed 5 rats in each group was determined by Western blots. Results The apoptotic index, levels of GRP78, CHOP, caspase 12 and phospho-p38 all showed significant differences （F=8.15, 12.28, 20.81, 18.63, 36.08, all P〈0.05）. All the indices in the model group and treatment group were higher than those in the sham-operation group, and were highest in the model group （all P 〈 0.05）. Conclusions Electroacupuncture pretreatment may inhibit endoplasmic reticulum stress and play a protective effect on myocardial ischemia reperfusion injury. The mechanism may be related to regulate phosphorylation of p38 signal pathway.