酸性成纤维细胞生长因子突变体对大鼠脑缺血再灌注损伤的保护作用。

Protective effects of mutant of acidic fibroblast growth factor against cerebral ischaemia-reperfusion injury in rats.

机构信息

Pharmacy College of Jinan University, Guangzhou, PR China.

出版信息

Injury. 2009 Sep;40(9):963-7. doi: 10.1016/j.injury.2009.01.110. Epub 2009 Jun 3.

DOI:10.1016/j.injury.2009.01.110

PMID:19497570

Abstract

OBJECTIVE

To investigate the protective effect of a mutant of acidic fibroblast growth factor (MaFGF) against cerebral ischaemia-reperfusion injury in rats.

METHODS

Sixty male Sprague-Dawley rats were randomly divided into six groups as follows: sham-operated group, untreated group, 20microg/kg, 40microg/kg and 80microg/kg MaFGF-treated groups and also the positive control group. Cerebral ischaemia-reperfusion injury was induced by middle cerebral artery occlusion (MCAO) for 2h followed by reperfusion for 24h. Different dose of MaFGF were infused intravenously at 1h after middle cerebral artery (MCA) occlusion. Nimodipine was used as positive control. The behaviour deficit score, brain-infarcted area, brain oedema degree, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were detected at 24h after reperfusion.

RESULTS

The results showed that MaFGF at the dose of 20microg/kg, 40microg/kg and 80microg/kg significantly alleviated brain injury. Compared to untreated group, the behaviour deficits were much less severe, the brain oedema alleviated obviously, the MDA contents decreased and SOD activity increased dramatically in MaFGF-treated groups respectively. The efficacy of MaFGF was similar to that of nimodipine.

CONCLUSION

The results demonstrate that MaFGF has neuroprotective effect against brain injury resulting from focal ischaemia-reperfusion in Sprague-Dawley rats.

摘要

目的

研究酸性成纤维细胞生长因子（MaFGF）突变体对大鼠脑缺血再灌注损伤的保护作用。

方法

60 只雄性 Sprague-Dawley 大鼠随机分为 6 组：假手术组、未治疗组、20μg/kg、40μg/kg 和 80μg/kg MaFGF 治疗组和阳性对照组。采用大脑中动脉闭塞（MCAO）2h 后再灌注 24h 的方法诱导脑缺血再灌注损伤。MCA 闭塞后 1h 静脉内给予不同剂量的 MaFGF。尼莫地平作为阳性对照。再灌注后 24h 检测行为缺陷评分、脑梗死面积、脑水肿程度、丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性。