Influence of ilexonin A on the expression of bFGF, GAP-43 and neurogenesis after cerebral ischemia-reperfusion in rats.
- Author:
Guan-yi ZHENG
1
;
Wang-qing SHI
;
Xiao-dong CHEN
;
Yuan-gui ZHU
;
Jing ZHANG
;
Qiong JIANG
Author Information
1. The Affiliated Union Hospital ofFujian Medical University, Fuzhou 350001, China. zhenggy2005@sina.com
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
drug effects;
Brain Ischemia;
etiology;
Bromodeoxyuridine;
metabolism;
Fibroblast Growth Factor 2;
metabolism;
GAP-43 Protein;
metabolism;
Infarction, Middle Cerebral Artery;
complications;
Male;
Neurogenesis;
drug effects;
Neurons;
pathology;
Neuroprotective Agents;
pharmacology;
Organic Chemicals;
pharmacology;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Reperfusion Injury;
etiology;
metabolism
- From:
Acta Pharmaceutica Sinica
2011;46(9):1065-1071
- CountryChina
- Language:Chinese
-
Abstract:
This study is to observe the effect of ilexonin A (IA) on the expression of basic fibroblast growth factor (bFGF) and growth associated protein-43 (GAP-43), and neurogenesis after cerebral ischemia-reperfusion in rats and explore its possible mechanism of protecting neuronal injury. Models of middle cerebral artery occlusion (MCAO) were established in SD rats. Before and after two hours ischemia-reperfusion, IA (20 and 40 mg x kg(-1)) was injected immediately and on 3, 7, 14, and 28 d once a day. The neurological severity was evaluated by neurological severity scores (NSS); neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Niss1 staining. The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blotting and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively. After treatment with IA, the NSS of treatment groups were lower than that of the models (3 and 7 d). The number of TUNEL positive neurons decreased and Nissl positive neurons increased at the same time (3 d). The expressions of bFGF and GAP-43 increased significantly in the boundary zone of the infarction area when compared to model group. Moreover, IA markedly enhanced the neurogenesis in the brain after ischemia-reperfusion, which revealed an increase of Brdu/NeuN positive cells in the boundary zone of the infarction area. The possible mechanism of protecting neuronal injury of IA may be related to inhibition on neuronal apoptosis, upregulation of bFGF and GAP-43, and neurogenesis in boundary zone of infarction after cerebral ischemia-reperfusion.
