Electroacupuncture alleviates acute myocardial ischemic injury in mice by regulating the β1 adrenergic receptor and post-receptor protein kinase A signaling pathway

Objective: To determine the effect of electroacupuncture (EA) on β 1 -adrenergic receptor (β 1 -AR) and post-receptor protein kinase A (PKA) signaling pathway after acute myocardial ischemia (MI). Methods: An MI model was established by ligating the left anterior descending coronary artery of wild-type (WT) C57/BL and β 1 -AR +/– mice (heterozygous for β 1 -AR gene deletion). EA treatment was administered at HT5-HT7 or LU9-LU8. We evaluated cardiac function by measuring ST segment displacement, ischemic area and serum levels of creatine kinase (CK)-MB and lactate dehydrogenase (LDH). Pathological morphology/apoptosis of myocardial tissue were examined using hematoxylin–eosin and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Norepinephrine (NE) levels in myocardial tissue were detected by ELISA. Levels of β 1 and post-receptor PKA signaling components were evaluated by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting. Results: EA stimulation at HT7-HT5 could better regulate the level of β 1 -AR in myocardial tissue than that at LU9-LU8. Following EA, the ST segment, serum CK-MB/ LDH and area of myocardial infarction were decreased in WT mice, and the degree of myocardial pathology/apoptosis and expression of cleaved caspase-3 were decreased. Myocardial levels of Gs protein (Gs), adenylate cyclase (AC), cyclic adenosine monophosphate (cAMP), phosphorylated protein kinase A (p-PKA), L-type voltage-gated calcium channel α1C (Cav1.2), serine phosphate 16-phospholamban (p-PLB s16 ) and sarcoplasmic reticulum Ca 2+ -adenosine triphosphate (ATP)ase 2a (SERCA2a) increased after EA. However, these effects of EA were not replicated in β 1 -AR +/– mice. Interestingly, myocardial NE content decreased after EA in WT and β 1 -AR +/– mice. Conclusion: EA may enhance cardiac function and reduced MI area/apoptosis by restoring the activity of β 1 -AR and post-receptor PKA signaling.