Objective To observe the effect of "Neiguan"(PC6)-electroacupuncture(EA)or moxibustion(Moxi)pretreatment on myocardial apoptosis and expression of autophagy related proteins light chain(LC)3-Ⅰand LC3-Ⅱin rats with myocardial ischemia/reperfusion injury(MIRI)

so as to explore their mechanisms underlying improvement of MIRI.Methods Forty SD rats(half male and half female)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"(PC6)for 20 min

once daily for 7 days.The MIRI 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 ultrastructural changes and autophagy of myocardial cells were observed by electron microscopy(EM)

and the myocardial cellular apoptosis[apoptotic index=(number of apoptotic cells/total number of cardiomyocytes)×100%]was detected by the terminal deoxyribonucleotidyl transferase mediated dUTP nick end labelling(TUNEL)method.The expressions of LC3-Ⅰand LC3-Ⅱproteins(markers for autophagy)in myocardial tissue were detected by Western blot.Results Following MI

EM observation revealed a vague structure of cardiomyocytes and muscular horizontal grain

dissolution of myofibers

mitochondrial swelling

some autophagic vacuoles and autophagic lysosomes at different degrees and surrounded by a double membrane in the model group

these situations were apparently milder in the EA and Moxi groups.The apoptosis index

myocardial LC3-Ⅰ and LC3-Ⅱ protein expression levels

and the ratio of LC3-Ⅱ/Ⅰwere significantly increased in the model group relevant to the sham operation group(P<0.05).After the treatment

the apoptosis index

the expression level of myocardial LC3-Ⅱ protein and the ratio of LC3-Ⅱ/Ⅰ were considerably down-regulated in the IP

EA and Moxi groups in comparison with those in the model group(P<0.05).The effect of EA was obviously superior to those of IP and Moxi in down-regulating the apoptosis index(P<0.05)

but obviously inferior to those of IP and Moxi in down-regulating the levels of LC3-Ⅱ and LC3-Ⅱ/Ⅰ(P<0.05).No significant changes were found in the expression of LC3-Ⅰ after IP

EA and Moxi interventions in comparison with the model group(P>0.05)

and no significant differences were observed in the apoptosis index and levels of LC3-Ⅱ and LC3-Ⅱ/Ⅰ between the IP and Moxi groups(P>0.05).Conclusion Both EA and moxibustion pretreatments

similar to IP

have a positive role in reducing myocardiocyte apoptosis and regulating autophagy-related protein expression in MIRI rats

which maybe contribute to their protective effects on ischemic myocardium.