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

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 response...

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Main Authors: Chun-ye Ma, Lin Yin
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2016-01-01
Series:Neural Regeneration Research
Subjects:
Online Access:http://www.nrronline.org/article.asp?issn=1673-5374;year=2016;volume=11;issue=7;spage=1102;epage=1107;aulast=Ma
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spelling doaj-f7a6b16371904a4eb9049e5bbd2230bc2020-11-25T03:36:04ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742016-01-011171102110710.4103/1673-5374.187044Neuroprotective effect of angiotensin II type 2 receptor during cerebral ischemia/reperfusionChun-ye MaLin YinAngiotensin 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.http://www.nrronline.org/article.asp?issn=1673-5374;year=2016;volume=11;issue=7;spage=1102;epage=1107;aulast=Manerve 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
collection DOAJ
language English
format Article
sources DOAJ
author Chun-ye Ma
Lin Yin
spellingShingle Chun-ye Ma
Lin Yin
Neuroprotective effect of angiotensin II type 2 receptor during cerebral ischemia/reperfusion
Neural Regeneration Research
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
author_facet Chun-ye Ma
Lin Yin
author_sort Chun-ye Ma
title Neuroprotective effect of angiotensin II type 2 receptor during cerebral ischemia/reperfusion
title_short Neuroprotective effect of angiotensin II type 2 receptor during cerebral ischemia/reperfusion
title_full Neuroprotective effect of angiotensin II type 2 receptor during cerebral ischemia/reperfusion
title_fullStr Neuroprotective effect of angiotensin II type 2 receptor during cerebral ischemia/reperfusion
title_full_unstemmed Neuroprotective effect of angiotensin II type 2 receptor during cerebral ischemia/reperfusion
title_sort neuroprotective effect of angiotensin ii type 2 receptor during cerebral ischemia/reperfusion
publisher Wolters Kluwer Medknow Publications
series Neural Regeneration Research
issn 1673-5374
publishDate 2016-01-01
description 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.
topic 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
url http://www.nrronline.org/article.asp?issn=1673-5374;year=2016;volume=11;issue=7;spage=1102;epage=1107;aulast=Ma
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AT linyin neuroprotectiveeffectofangiotensiniitype2receptorduringcerebralischemiareperfusion
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