Time-dependent Protective Effect of Electroacupuncture on Ischemic Myocardium and Changes of Myocardial Autophagy and Apoptosis Related Protein Expression in Rats / 针刺研究

ABSTRACT

OBJECTIVE: To observe the effect of electroacupuncture (EA) at different time-points on the injured myocar-dium and expression of myocardial Bax/Bcl-2 and Lc 3 Ⅱ/Ⅰ proteins in acute myocardial ischemia-reperfusion injury (MIRI) rats so as to explore its mechanisms underlying myocardial protective effect via reducing cardiomyocyte autophagy and apoptosis. METHODS: A total of 66 adult SD rats were randomly divided into sham operation (sham), model, EA-R 0min(R＝ reperfusion), EA-R 30min, EA-R 60min, and EA-R 120min groups, with 6 rats being in the sham group and 12 rats being in each of the other 5 groups. The MIRI model was prepared by ligating the anterior descending branch (ADB) of the left coronary artery for 30 min followed by reperfusion for 4 h. In the sham group, the ADB was only threaded without ligation. EA was applied to bilateral "Neiguan" (PC 6) for 20 min at 0, 30, 60, and 120 min when reperfusion. Evans Blue-triphenyltetrazolium chloride (TTC) double staining was performed to determine the myocardial infarction area (MIA) and the ratio of the infarct size of the area at risk (IS/AAR). ELISA was performed to measure serum cardiac troponin 1 (cTn-Ⅰ) content, and Western blot was used to measure the expression of apoptosis-related proteins Bax and Bcl-2 and autophagy related proteins Lc 3 Ⅱ and Lc 3 Ⅰ in the left cardiac ventricle tissue. RESULTS: Compared with the model group, the percentages of MIA in the EA-R 30min, EA-R 60min, and EA-R 120min groups, and the IS/AAR in the EA-R 0min, EA-R 30min, EA-R 60min and EA-R 120min groups were significantly reduced (P0.05). CONCLUSION: EA intervention can reduce MIA in MIRI rats, which is possibly closely related to its effects in reducing apoptosis and autophagy. The best intervention time is at 30 min after MI reperfusion, but the difference of effects of EA at different time-points is independent of Bax/Bcl-2 and Lc 3 Ⅱ/Ⅰ expression.