Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment-Induced Cardioprotection against Ischemia-Reperfusion Injury in Rats

Figure 7

Effects of CB1R and CB2R signaling on propofol conditioning induced antioxidation in vivo. Rat myocardial ischemia/reperfusion (I/R) injury model was set up by ligating left descending coronary artery for 30 minutes and loosening for 24-hour reperfusion. Before and during ischemia, propofol was continuously infused. Selective CB1R antagonist AM251 (1 mg/kg) or selective CB2R antagonist AM630 (1 mg/kg) was injected intravenously 30 minutes before propofol exposure. Serum SOD activities (a), MDA concentrations (b), and MPO concentrations (c) were detected 24 hours after 24-hour reperfusion. The results showed that propofol conditioning was cardioprotective through decreasing oxidation injury. The antioxidative effects of propofol were fully reversed by pretreatment with AM630. per group. : ; : versus sham. #: ; ##: versus I/R. ††: versus propofol + I/R. ‡‡: versus AM251 + I/R. §§: versus AM251 + propofol + I/R.

(a) Serum SOD

(b) Serum MDA

(c) Serum MPO