The effects of basic fibroblast growth factor on neuronal apoptosis in the hippocampus of epileptic rats
孙钦建, 迟兆富, Tao Zhang, 王爱华, 段瑞生, 张秀清
Abstract
孙钦建, 迟兆富, Tao Zhang, 王爱华, 段瑞生, 张秀清
Abstract
Objective To investigate the neuroprotective effects of basic fibroblast growth factor (bFGF) on epileptic rats and the possible mechanisms. Methods Rats with pentylenetetrazol-induced seizures were randomly divided into the bFGF group (intraperitoneally injected with bFGF at the daily frequency) and NS group (control group, intraperitoneally injected with normal saline at the daily frequency), 36 rats in each group; all the rats were executed at 6 h, 12 h, 24 h, 2 d, 3 d and 5 d after seizures and their heads were removed; the removed brain tissues were then sliced to undergo immunohistochemical staining, which was performed to observe the expressions of bcl-2 and caspase-3, and the terminal deoxynucletidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), which was used to detect the apoptotic cells ofhippocampal neurons. Results Bcl-2, caspase-3 and TUNEL staining: differences of positive expressions in hippocampal CA1 and CA3 regions 6 h after seizures were not significant between the bFGF and NS groups (P〉0.05); the positive expressions increased gradually during 12 h and 48 h, when the expressions of bcl-2 and TUNEL-positive cells were significantly higher in the bFGF group than that in the NS group and the caspase-3 expression in the bFGF group was significantly lower than that in the NS group, so the differences had statistical significance (P〈0.01 ,P〈 0.001); the positive expressions decreased 3 d later after seizures and differences between the bFGF and NS groups had no statistical significance (P 〉0.05). Conclusion The injection of bFGF can remarkably reduce the hippocampal neuronal apoptosis induced by seizures, indicating that regulating the expressions of bcl-2 and caspase-3 and inhibiting neuronal apoptosis may exert the neuroprotective effects of bFGF. Key words: Epilepsy; Basic fibroblast growth factor; Bcl-2; Caspase-3; Apoptosis
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Objective To investigate the neuroprotective effects of basic fibroblast growth factor (bFGF) on epileptic rats and the possible mechanisms. Methods Rats with pentylenetetrazol-induced seizures were randomly divided into the bFGF group (intraperitoneally injected with bFGF at the daily frequency) and NS group (control group, intraperitoneally injected with normal saline at the daily frequency), 36 rats in each group; all the rats were executed at 6 h, 12 h, 24 h, 2 d, 3 d and 5 d after seizures and their heads were removed; the removed brain tissues were then sliced to undergo immunohistochemical staining, which was performed to observe the expressions of bcl-2 and caspase-3, and the terminal deoxynucletidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), which was used to detect the apoptotic cells ofhippocampal neurons. Results Bcl-2, caspase-3 and TUNEL staining: differences of positive expressions in hippocampal CA1 and CA3 regions 6 h after seizures were not significant between the bFGF and NS groups (P〉0.05); the positive expressions increased gradually during 12 h and 48 h, when the expressions of bcl-2 and TUNEL-positive cells were significantly higher in the bFGF group than that in the NS group and the caspase-3 expression in the bFGF group was significantly lower than that in the NS group, so the differences had statistical significance (P〈0.01 ,P〈 0.001); the positive expressions decreased 3 d later after seizures and differences between the bFGF and NS groups had no statistical significance (P 〉0.05). Conclusion The injection of bFGF can remarkably reduce the hippocampal neuronal apoptosis induced by seizures, indicating that regulating the expressions of bcl-2 and caspase-3 and inhibiting neuronal apoptosis may exert the neuroprotective effects of bFGF. Key words: Epilepsy; Basic fibroblast growth factor; Bcl-2; Caspase-3; Apoptosis
Key concepts: TUNEL assay, Basic fibroblast growth factor, Hippocampal formation, Endocrinology, Apoptosis, Internal medicine, Immunohistochemistry, Neuroprotection