Regulating effect of electroacupuncture on left ventricular function and autophagy-specific proteins in spontaneously hypertension rats / 针刺研究

ABSTRACT

OBJECTIVE: To investigate the effect of electroacupuncture (EA) on cardiac hypertrophy and expression of myocardial autophagy-specific proteins in spontaneously hypertensive rats (SHRs). METHODS: Twelve male Wistar Kyoto (WKY) rats were selected as the normal control group, and 24 male SHRs were randomized into model and EA groups (n＝12 in each). EA (2 Hz /15 Hz, 1 mA) was applied to "Taichong" (LR3) and "Baihui" (GV20) for 20 min, once a day for successive 30 days. The other two groups only received the same grasping and fixation procedures. The systolic blood pressure (SBP) was measured using a non-invasive blood detector, and the left ventricular function including the left ventricular anterior wall diameter (LVAWd), left ventricular posterior wall diameter (LVPWd) and left ventricular internal diameter at end-diastolic dimension (LVIDd) was detected using a real-time echocardiography imaging system, and the left ventricular mass index (left ventricle weight / body weight, LVMI) was calculated. The expression of Beclin-1 and LC3 proteins in the left ventricle tissue was detected by Western blot. Pathological changes of the myocardial tissue were observed by Masson staining and transmission electron microscope (TEM). RESULTS: After the intervention, the elevated SBP was significantly lowered in the EA group relevant to the model group (P<0.01) and the increased LVAWd, LVPWd and LVMI were markedly decreased in the EA group (P<0.01, P<0.05), while the reduced LVIDd was significantly ameliorated in the EA group (P<0.01). Masson staining showed that in SHRs, disorder of arrangement of cardiac myofibers, swelling of cardiomyocytes, widened space among myocardial cells with a large number of collagenous fibers were observed, and under TEM, aggregation and unequal size of myocardial mitochondria with vacuolation and rupture, autophagosomes and autophagic lysosomes were seen. These changes were relatively milder in the EA group. Western blot showed that hypertension induced up-regulation of Beclin-1 and LC3-II and ratio of LC3-II/LC3-I, and down-regulation of LC3-I were significantly suppressed in the EA group (P<0.01, P<0.05). CONCLUSION: EA at LR3 and GV20 may improve the left cardiac function, myocardial morphological changes and the degree of autophagy in SHRs, which is related to its effects in down-regulating the expression of myocardial Beclin-1 and LC3-II and in up-regulating expression of LC3-I.