中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (7): 1102-1107.doi: 10.4103/1673-5374.187044

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

脑缺血再灌注过程中AT2受体的神经保护作用

  

  • 出版日期:2016-07-30 发布日期:2016-07-30

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

Chun-ye Ma, Lin Yin*   

  1. Department of Neurology, the Second Hospital of Dalian Medical University, Dalian, Liaoning Province, China
  • Online:2016-07-30 Published:2016-07-30
  • Contact: Lin Yin, M.D., andreas2005@vip.sina.com.

摘要:

动物实验已证实,AT2受体的活化对脑卒中起保护作用,但具体机制不明。实验假设AT2受体保护脑缺血再灌注损伤的作用是通过抑制免疫炎症反应而实现的,故将大脑中动脉闭塞大鼠模型分别腹腔注射生理盐水,AT2受体激动剂CGP42112(1 mg/(kg.d))和AT2受体阻滞剂PD123319(1 mg/(kg.d))。发现与盐水对照组比较,给予AT2受体激动剂CGP42112处理大鼠脑组织中AT2受体表达量增加,脑梗死体积缩小,脑组织中白细胞介素1β和肿瘤坏死因子α表达减少,白细胞介素10表达增加;给予AT2受体阻滞剂PD123319处理后则得到相反效果,结果证明,AT2受体抑制免疫炎症反应而起到了保护脑缺血再灌注损伤的作用。 

orcid: 0000-0003-3912-9584 (Lin Yin)

关键词: 神经再生, 脑损伤, 脑缺血再灌注, AT2受体, 白细胞介素1β, 肿瘤坏死因子α, 白细胞介素10, 大脑中动脉闭塞模型, 脑梗死体积, CGP42112, PD123319, 免疫炎症反应

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."

Key words: 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