Fig. 7
From: Resolvin D2 protects against cerebral ischemia/reperfusion injury in rats
Mode pattern illustrating the possible mechanisms of RvD2’s alleviation of cerebral ischemic and reperfusion injury. The intracellular ROS in neurons and endothelial cells were active and induced cell apoptosis and cerebral injury after MCAO/R induction. Extracellular 17-HDHA generated RvD2 depending on the phosphorylation of 5-LOX. RvD2 bound to its receptor GPR18 in the plasma membrane and triggered intracellular signal transduction through phosphorylation of ERK1/2, followed by stimulating nNOS or eNOS to suppress neuronal or endothelial cells apoptosis and induced an increase of tight junction protein ZO-1 to maintain BBB integrity. This pathologic process alleviated early brain injury after MCAO/R