Electroacupuncture pre-treatment ameliorates myocardial ischaemia/reperfusion injury through regulation of cannabinoid receptor type 2

Abstract

Electroacupuncture (EA) therapy has widely been accepted as a useful therapeutic technique with low risk in the clinical setting for prevention from cardiac disease. However, the physiological mechanism under which this protective effect works remains unclear. The present study investigated the effects of EA pretreatment on myocardial ischaemia/reperfusion (MI/R) injury in mice and its possible signalling pathway. Mice were randomly divided into Sham, MI/R, EA + MI/R, EA(−) + MI/R, and AM630 + EA + MI/R groups. We reported that EA pretreatment significantly ameliorated MI/R injury, evidenced by increased cardiac function, reduced infarct size, and decreased apoptosis. This was associated with a reduction of oxidative stress in the infarcted myocardium, which was through CB2. The CB2 expression was up-regulated in the heart after EA pretreatment, as well as heart tissue content of N -arach-idonoylethanolamine-anandamide and 2-arachidonylglycerol. Furthermore, the expression of adenosine monophosphate-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) in the left ventricular myocardial tissue was decreased in the MI/R group, whereas increased in the EA pretreatment group. Administration of AM630 before EA pretreatment did not improve cardiac function and inhibit oxidative stress. Preinjection of AM630 or AMPK inhibitor compound C could partially decrease the expression of EA pretreatment-mediated AMPK or PGC-1α. Pretreatment with EA increased the production of endocannabinoid, which elicited protective effects against MI/R injury through CB2 activation. The mechanism of this effect was related to the activation of AMPK/PGC-1α pathway, followed by an inhibition of oxidative stress.