Neuroprotective effect of angiotensin II type 2 receptor during cerebral ischemia/reperfusion

Abstract

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 AT2R 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 AT2R agonist CGP42112 (1 mg/kg per day) or antagonist PD123319 (1 mg/kg per day). In the CGP42112 group, AT2R 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 AT2R using PD123319 produced the opposite effects. These results indicate that AT2R activation suppresses immune and inflammatory responses, and protects against cerebral ischemia/reperfusion injury.

Keywords

• nerve regeneration; brain injury; cerebral ischemia/reperfusion; angiotensin II type 2 receptor; interleukin-1β; tumor necrosis factor-α; interleukin-10; middle cerebral artery occlusion; infarct area; CGP42112; PD123319; immune and inflammatory responses; neural regeneration