Electroacupuncture for myocardial ischemia injury in rats via AMPK-HDAC5-HIF-1α signaling

Abstract

To explore the impact of electroacupuncture (EA) on the AMPKα-HDAC5-HIF-1α signaling in the heart of the rats with myocardial ischemia (MI) via detecting the expressions of AMP-activated protein kinase α (AMPKα), histone deacetylase 5 (HDAC5), hypoxia inducible factor (HIF-1α) and vascular endothelial growth factor (VEGF). Thirty-six healthy male SD rats were randomized into a sham operation group (6 rats), a sham + EA group (6 rats), a model group (12 rats) and an EA group (12 rats). We ligated the left anterior descending artery (LAD) for MI model, and exposed the heart of rats after opening the chest without ligation for the rats in the sham operation gorup and the sham + EA group. On the 2nd day after LAD ligation, EA was applied at "Neiguan" (PC 6) with 2 Hz/15 Hz and 1.5-2 mA for 30 min in the EA group and sham+EA group, once a day for 4 days. The same fixation was used in the sham operation group and the model group, without EA. Myocardial infarction area was observed by TTC staining and serum cardiac troponin T (cTnT) was detected by radioimmunoassay. The expression of VEGF mRNA was detected by real time PCR. The protein expressions of AMPKα, HDAC5, HIF-1α and VEGF were detected by western blot. Compared with the sham operation group, 4 days after LAD ligation, the myocardial infarction was obvious and the expression of serum cTnT increased in the model group (P<0.01); and the proterin expression of HIF-1α in myocardial tissue ascended (P<0.01); the expression of VEGF mRNA decreased (P<0.05); the changes of the protein expressions of AMPKα、HDAC5、VEGF were not obvious (all P>0.05). After EA for 4 days, the myocardial infarction area and cTnT expression decreased in the EA group (both P<0.01); the VEGF mRNA and protein expressions and AMPKα, HDAC5, HIF-1α protein expressions increased (P<0.05, P<0.01). EA could regulate the AMPKα-HDAC5-HIF-1α signaling in myocardial tissue, which may activate VEGF expression for angiogenesis signaling, reduce myocardial infarction area so as to achieve cardioprotective effect.