Neuroprotective effect of angiotensin-(1-7) against focal cerebral ischemic-reperfusion injury in rats
10.3760/cma.j.issn.1671-8925.2008.05.003
- VernacularTitle:血管紧张素-(1-7)对大鼠局灶性脑缺血再灌注损伤的神经保护作用
- Author:
Jie LU
1
;
Ying-Dong ZHANG
;
Jing-Ping SHI
;
Jing-De DONG
;
Xing-Jian LIN
Author Information
1. 南京医科大学附属脑科医院
- Keywords:
Angiotensin-(1-7);
Cerebral infaction;
Reperfusion injury;
Apoptosis
- From:
Chinese Journal of Neuromedicine
2008;7(5):440-444
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effects ofAngiotensin-(1-7) [Ang-(1-7)] against the focal cerebral ischemic-reperfusion injury in rats. Methods Spragne-Dawley rats were randomly divided into sham operated group, Ang-(1-7) treated group and aCSF treated group. The latter 2 groups were subjected to middle cerebral artery occlusion (MCAO). The 3 groups were administrated artificial cerebrospinal fluid (aCSF, 0.5 μL/h), Ang-(1-7) (100 pmol, 0.5 μL/h) and aCSF 0.5 μL/h,respectively, by implanted Alzet osmotic minipumps into lateral cerebral ventricle at reperfusion 24 h and 48 h. In all experimental rats, their neurological function scores, the brain edema at reperfusion 48 h and the cerebral infarct size at reperfusion 24 h were evaluated. And the malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in the ischemic cerebral tissue at reperfusion 24 h and 48 h were also determined. The number of apoptotic neurons within the tissue around the infarct at reperfusion 48 h was detected by the way of staining with terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick-end labeling (TUNEL). Results In the treatment of MCAO rats, Ang-(1-7) significantly ameliorated their neurological function score (P＜0.05), reduced the infarct size (P＜0.05), decreased the tissue MDA content (P＜0.05), increased the tissue SOD activity (P＜0.05). It also reduced markedly the number of apoptotic neurons around the infarct (P＜0.01), but had no effect on the water content in the brain. Conclusions Ang- (1-7) has a neuroprotective effect against cerebral ischemic-reperfusion injury, perhaps by its anti-oxidation stress and inhibition of neuronal apoptosis.
