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.