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 β1-adrenergic receptor (β1-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 β1-AR+/- mice (heterozygous for β1-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 β1 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 β1-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-PLBs16) and sarcoplasmic reticulum Ca2+-adenosine triphosphate (ATP)ase 2a (SERCA2a) increased after EA. However, these effects of EA were not replicated in β1-AR+/- mice. Interestingly, myocardial NE content decreased after EA in WT and β1-AR+/- mice.

CONCLUSION

EA may enhance cardiac function and reduced MI area/apoptosis by restoring the activity of β1-AR and post-receptor PKA signaling.