摘要
Angiotensin Ⅱ type 2 receptor（AT2R） activation has been shown to protect against stroke,but its precise mechanism remains poorly understood.We investigated whether the protective effect of AT2 R against ischemia/reperfusion injury is mediated by the suppression of immune and inflammatory responses.Rat models of middle cerebral artery occlusion were intraperitoneally injected with physiological saline,the AT2 R agonist CGP42112（1 mg/kg per day） or antagonist PD123319（1 mg/kg per day）.In the CGP42112 group,AT2 R expression increased,the infarct area decreased,interleukin-1β and tumor necrosis factor-α expression decreased,and interleukin-10 expression increased compared with the saline group.Antagonisin AT2 R using PD123319 produced the opposite effects.These results indicate that AT2 R activation suppresses immune and inflammatory responses,and protects against cerebral ischemia/reperfusion injury.
Angiotensin Ⅱ type 2 receptor（AT2R） activation has been shown to protect against stroke,but its precise mechanism remains poorly understood.We investigated whether the protective effect of AT2 R against ischemia/reperfusion injury is mediated by the suppression of immune and inflammatory responses.Rat models of middle cerebral artery occlusion were intraperitoneally injected with physiological saline,the AT2 R agonist CGP42112（1 mg/kg per day） or antagonist PD123319（1 mg/kg per day）.In the CGP42112 group,AT2 R expression increased,the infarct area decreased,interleukin-1β and tumor necrosis factor-α expression decreased,and interleukin-10 expression increased compared with the saline group.Antagonisin AT2 R using PD123319 produced the opposite effects.These results indicate that AT2 R activation suppresses immune and inflammatory responses,and protects against cerebral ischemia/reperfusion injury.
