Abstract

Electroacupuncture (EA) can improve myocardial ischemia (MI) injury; nevertheless, the mechanism is not entirely clear. And there were disagreements about whether the effect of EA at acupoint in disease-affected meridian is better than EA at acupoint in non-affected meridian and sham acupoint. Here, we showed that the effect of EA at Neiguan (PC6) is better than EA at Hegu (LI4) and sham acupoint in affecting RPP and ECG, increasing ATP and ADO production, decreasing AMP production, and upregulating the mRNA expression levels of A1AR, A2aAR, and A2bAR; knockdown of A1AR or A2bAR reversed the effect of EA at PC6 in alleviating MI injury; knockdown of A2aAR had no influence on the cardiac protection of EA at PC6; thus, the cardioprotective effect of EA at PC6 needs A1AR and A2bAR, instead of A2aAR; considering that the cardio protection of adenosine receptor needs activation of other adenosine receptors, one of the reasons may be that after silence of A1AR or A2bAR, EA at PC6 could not impact the expression levels of the other two adenosine receptors, and after silence of A2aAR, EA at PC6 could impact the expression levels of A1AR and A2bAR. These results suggested that EA at PC6 may be a potential and effective treatment for MI by activation of A1AR and A2bAR.

Highlights

  • Myocardial ischemia (MI) is one of heart conditions caused by lack of coronary blood flow [1], which is the primary cause of ischemic heart disease (IHD)

  • The results showed that MI injury caused decrease in the concentrations of ATP and ADO and increase in the concentration of AMP (Fig. 3a–d, all P < 0.01) and no change in the concentration of ADP (Fig. 3c, all P > 0.05) compared with the normal control (NC) group and the sham operation (SO) group

  • Our results indicated that (a) EA at PC6 has better effect than EA at LI6 and sham acupoint in affecting rate pressure product (RPP) and ECG, increasing ATP and ADO production, decreasing AMP production, and upregulating the expression levels of A1 adenosine receptor (A1AR), A2a adenosine receptor (A2aAR), and A2b adenosine receptor (A2bAR); (b) A1AR and A2bAR are involved in EA-induced cardio protection in MI injury; and (c) silence of A1AR or A2bAR reverses the influence of EA at PC6 in upregulating the other two adenosine receptors and silence of A2aAR has no influence on the effect of EA at PC6 in upregulating A1AR and A2bAR

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Summary

Introduction

Myocardial ischemia (MI) is one of heart conditions caused by lack of coronary blood flow [1], which is the primary cause of ischemic heart disease (IHD). The “The top 10 causes of death” indicated that IHD is one of the biggest killers in the world, accounting for around 9 million death in 2016 [2]. “Guideline on the Assessment and Management of Cardiovascular Risk in China,” which was published in 2019, showed that cardiovascular disease is the leading cause of death and burden of disease in China, and over 1 million people died of coronary heart disease [3]. The primary therapeutic methods include percutaneous coronary intervention, coronary artery bypass grafting, and medical therapy [5,6,7,8,9,10,11].

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