目的探讨电针(EA)预处理抗心肌缺血再灌注(I/R)损伤及其大鼠MAPK信号通路的影响。方法 SD大鼠随机分为6组:假手术组(SO)、电针内关穴+SO组(ES)、电针非经非穴+SO组(NS)、I/R组(I/R)、电针内关穴+I/R组(EA)、电针非经非穴+I/R组(NA),每组6只。ES、EA电针内关穴,NS、NA电针鼠尾,连续治疗12d后造模。I/R、EA、NA组均结扎左前降支建立心肌I/R模型,SO、ES、NS组均开胸不结扎。手术过程中监测心电图,测血清肌酸激酶同工酶(CK-Mb),用Western blot检测MAPK信号通路相关蛋白的表达水平。结果与SO组比较,I/R组大鼠血清CK-Mb水平、心律失常评分、蛋白PSAPK/JNK、P-P44/42和Ras表达均增加(P〈0.05),而P-P38水平减低(P〈0.05)。与I/R组比较,EA、NA组CK-Mb水平均降低,EA组心律失常评分明显减少(P〈0.05),EA、NA组P-P44/42和Ras表达均下调(P〈0.05),而P-P38水平增高(P〈0.05)。结论电针预处理能有效保护心肌抗I/R损伤,该效应可能与其调节受损心肌组织中MAPK信号通路密切相关。
OBJECTIVE To investigate the electro-acupuncture pretreatment on myocardial ischemia-reperfusion(I/R)injury in rats and its effects on MAPK pathway.METHODS Thirty-six SD rats were randomly divided into six groups(6in each):sham operation group(SO),electro-acupuncture at PC6with SO group(ES),electro-acupuncture at non-acupoint with SO group(NS),I/R group(I/R),electro-acupuncture at PC6with I/R group(EA)and electro-acupuncture at non-acupoint with I/R group(NA).Electro-acupuncture at PC6was applied to ES and EA groups,and electro-acupuncture at non-acupoint area on the tail of the rats was given to NS and NA groups both for 12days,after which the modeling operations were carried out.In the operation,the left anterior descending coronary artery(LAD)of the rats was occluded in I/R,EA and NA groups and thoracotomy without LAD ligation was performed in SO,ES and NS groups.ECG was monitored during the operation and CK-Mb in serum was measured after the reperfusion.The expression of MAPK pathway proteins was tested with Western blot.RESULTS Compared with SO group,I/R group had a significant increase(P〈0.05)in serum CK-Mb,arrhythmia score,P-P44/42,P-SAPK/JNK and Ras protein expressions,but a decrease in P-P38level(P〈0.05).In contrast to I/R group,EA and NA groups had a decrease in P-P44/42and Ras expression(P〈0.05),as well as in serum CK-Mb level,but witnessed a significant increase in P-P38level(P〈0.05).However,the arrhythmia score in EA group significantly decreased(P〈0.05).CONCLUSION Electro-acupuncture pretreatment can effectively protect the myocardium in I/R injury possibly by its regulation of MAPK pathway existed in damaged cardiac tissues.