Objective To observe the effect of electroacupuncture(EA)and moxibustion(Moxi)pretreatment on myocardial pathological and structural changes and expression of autophagy related protein LC 3 Ⅰ/Ⅱ and Beclin 1 in rats with myocardial ischemia-reperfusion injury(MI/RI)

so as to explore their mechanisms underlying improving MI/RI.Methods Forty SD rats were randomly divided into sham operation

model

ischemic preconditioning(IP)

EA and Moxi groups(n=8 in each group).EA(10 Hz/50 Hz

1 mA)or Moxi(ignited moxa stick)was respectively applied to bilateral"Neiguan"(PC 6)for 20 min

once daily for 7 days.The MI/RI model was established by occlusion of the anterior descending branch of the left coronary artery for 40 min

followed by reperfusion for 60 min.The left ventricular(LV)tissue samples were collected and analyzed for pathological(H.E.staining)and ultrastructural changes

for myocardial apoptosis(apoptotic index= number of apoptotic cells/total number of cardiomyocytes×100%)with terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL)method

and for the expression of LC 3 and Beclin 1 in myocardial cells with Western blot.Results Following MI/RI

H.E.staining revealed a disorder of arrangement of cardiomyocytes with vague border

inflammatory cell infiltration

intracellular swelling with bleeding

necrosis and dissolution of partial striated muscles of the left ventricle under light microscope

and dual staining of Uranyl acetate and leadnitrate showed atrophy

arrangement disorder

dissolution

necrosis

and interstitial edema of partial myocardial fibers

mitochondrial structural disorder

vacolation

and large body of autophagosomes with bilayers

etc.in ultrastructure

which was relatively lighter in both EA and Moxi groups.The apoptosis index

expression levels of myocardial LC 3Ⅱ and Beclin 1 and the ratio of LC 3 Ⅱ/LC 3 Ⅰ were significantly higher in the model group than those in the sham operation group(P<0.01)

but the expression level of LC 3 Ⅰ was considerably down-regulated in the model group relevant to the sham operation group(P<0.01).Following the intervention and MI preconditioning

the increased apoptosis index and expression levels of LC 3Ⅱ and Beclin 1 proteins and the ratio of LC 3Ⅱ/LC 3 Ⅰ were obviously down-regulated in the IP

EA and Moxi groups relevant to the model group(P<0.01)

and the decreased expression of LC 3 Ⅰ protein was up-regulated obviously in the 3 treatment groups(P<0.05

P<0.01).The effects of EA were significantly superior to those of IP and Moxi groups in down-regulating apoptosis index and expression of LC 3Ⅱand Beclin 1 and the ratio of LC 3Ⅱ/LC 3Ⅰand in up-regulating expression of LC 3Ⅰ(P<0.05

P<0.01).Conclusion Both EA and Moxi preconditioning of PC 6 have a protective effect on ischemic myocardium in MI/RI rats

which is probably related to their effects in regulating expression of myocardial autophagy proteins as LC 3 Ⅰ/Ⅱ and Beclin 1.