论文部分内容阅读
OBJECTIVE:To investigate the protective efficacy of electroacupuncture(EA)pretreatment at Nei-guan(PC6)on myocardial ischemia-reperfusion(I/R)in rats.METHODS:Fifty rats were randomly divided into five groups(n = 10):sham operation group,model group(underwent in vivo myocardial I/R),EA pre-treatment group[EA at Neiguan(PC 6)1 week be-fore I/R],wortmannin group(1 week before l/R,the PI3K inhibitor,wortmannin,was injected),EA pre-treatment+wortmannin group(both pretreat-ments were performed simultaneously).After es-tablishing the I/R model,2,3,5-triphenyltetrazolium chloride(TTC)staining was used to analyze the weight and area of the myocardial infarction tissue.The biosignal and pressure test system was used to determine the left ventricular systolic mean pres-sure(LVSP),left ventricular end-diastolic pressure(LVEDP),fractional shortening(FS),and ejection fraction(EF).Ultraviolet spectrophotometry was used to determine the expression of creatine ki-nase(CK)-MB,inducible nitric oxide synthase(iN-OS),and total antioxidant capacity(T-AOC)in the serum.The expression of autophagy-related pro-tein 13(ATG13),mammalian target of rapamycin(mTOR),and phosphatidylinositol 3-kinase(PI3K)in cardiac muscle cells was determined by immunoflu-orescence.Hematoxylin and eosin staining was used to observe autophagy-related pathological changes in rat cardiomyocytes,and ultrastructural changes of cardiomyocytes were examined by transmission electron microscopy.RESULTS:In this study,the infarction size and tis-sue weight of the EA pretreatment group were de-creased compared with the model group(P＜0.0001).Furthermore,compared with the model group,the LVEDP values of the EA pretreatment group were significantly reduced(P = 0.0091),and the LVSP,FS,and EF values were slightly increased(P = 0.0007,0.0020,0.0031).EA pretreatment also significantly decreased the expression of CK-MB and iNOS,while it increased the expression of T-AOC in the serum of rats with I/R injury(P＜0.0001).Furthermore,EA pretreatment slightly wid-ened the myocardial fiber space,reduced necrosis and myocardial cell swelling and maintained the nucleus and mitochondria structure intact.CONCLUSION:EA pretreatment promoted autoph-agy flux and alleviated myocardial I/R injury through the PI3K-Akt-mTOR pathway.