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

Figure 5

Effects of propofol conditioning, URB pretreatment, and VDM11 pretreatment on cardiomyocyte MDA concentrations (a), SOD concentrations (b), and ROS productions (c). In the in vitro cardiomyocyte hypoxia/reoxygenation (H/R) model, propofol (50 μM) was incubated to achieve cardioprotection. Selective FAAH inhibitor URB597 and endocannabinoid reuptake inhibitor VDM11 were further used to increase endocannabinoid levels before propofol conditioning. The results showed that propofol conditioning was cardioprotective through decreasing oxidation (a and c). URB597 and VDM11 mimic the effects of propofol conditioning. The cardioprotective effects of propofol could not be exerted when URB597 or VDM11 was pretreated. per group. : ; : versus control. ##: versus propofol. ††: versus H/R.

(a) Cell MDA

(b) Cell SOD

(c) Cell ROS