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Updated: May 11, 2026
Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
Published on: March 1, 2019
[The expression of bFGF, GAP-43 and neurogenesis after cerebral ischemia/reperfusion in rats]
Wang-Qing Shi1, Guan-Yi Zheng, Xiao-Dong Chen
1The Affiliated Union Hospital of Fujian Medical University, Fuzhou 350001, China.
Objective:
To observe time points of the expressions of basic fibroblast growth factor (bFGF), growth associated protein-43 (GAP-43) and neurogenesis after cerebral ischemia/reperfusion in rats and explore its possible mechanism of neurogenesis.
Methods:
Models of middle cerebral artery occlusion (MCAO) were established in SD rats which were divided into 3 d, 7 d, 14 d and 28 d groups (n = 6). The neurological severity was evaluated by neurological severity scores (NSS) and scores of motor test (SMT). Neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Nissl staining; The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blot and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively.
Results:
It showed up neurologic impairment and motor dysfunction after cerebral ischemia/reperfusion in rats at 3 d, the numbers of neuron apoptosis also peaked at 3d, the protein levels of bFGF and GAP-43 were significantly increased in time-dependent manner, peaked at 7 d and then decreased gradually, meanwhile, Brdu and NeuN double fluorescence staining displayed scattered Brdu-and NeuN-positive cells in the boundary zone of the infarction area.
Conclusion:
These results suggest that the upregulation of bFGF and GAP-43 may contribute to the neurogenesis after cerebral ischemia/reperfusion.
