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目的探讨碱性成纤维细胞生长因子(bFGF)对致痫大鼠的神经保护作用及可能机制。方法给予戊四氮(PTZ)致痫大鼠每日腹腔注射bFGF(bFGF组,n=36)、生理盐水(NS组,n=36),分别于痫性发作后6h、12h、24h、48h、3d、5d处死取脑,切片进行bcl-2、caspase-3染色,用原位末端标记(TUNEL)方法检测海马神经元凋亡细胞。结果痫性发作6h后两组海马CA1、CA3区的bcl-2、caspase-3、TUNEL染色阳性表达差异无统计学意义(P>0.05);12～48 h表达逐渐增强,bFGF组bcl-2、TUNEL的表达显著高于NS组,bFGF组caspase-3的表达显著低于NS组(P均<0.01);3d后表达减弱.bFGF组与NS组的差异无统计学意义(P>0.05)。结论bFGF能显著减轻癫痫所致的海马神经元凋亡,提示可能通过调控bcl-2和caspase-3基因的表达发挥作用。
Objective To investigate the neuroprotective effect of basic fibroblast growth factor (bFGF) on epileptic rats and its possible mechanism. Methods Rats with epileptic seizures induced by pentylenetetrazol (PTZ) were intraperitoneally injected with bFGF (bFGF, n = 36) and normal saline (n = 36) respectively at 6h, 12h, 24h and 48h after epileptic seizure The brain slices were sacrificed on day 3, day 5 and day 5, and bcl-2 and caspase-3 were stained. The apoptosis of hippocampal neurons was detected by TUNEL. Results The expressions of bcl-2, caspase-3 and TUNEL in hippocampal CA1 and CA3 were not significantly different at 6h after epileptic seizure (P> 0.05), and gradually increased at 12-48 h , While the expression of TUNEL in NSCLC was significantly higher than that in NS group (P <0.05). The expression of caspase-3 in bFGF group was significantly lower than that in NS group (P <0.01) . Conclusion bFGF can significantly reduce the apoptosis of hippocampal neurons induced by epilepsy, suggesting that bFGF may play a role in regulating the expression of bcl-2 and caspase-3 genes.