经鼻给予TGFβ1对氯化锂-匹罗卡品诱导的SE大鼠海马神经元凋亡调控因子Bcl-2、Bax蛋白表达的影响

目的探讨经鼻给予TGFβ1(Transforming growth factor-beta1,TGFβ1)对氯化锂-匹罗卡品诱导的癫痫持续状态(status epilepticus,SE)大鼠海马神经元凋亡调控因子Bcl-2、Bax蛋白表达的影响。方法健康雄性SD大鼠60只,随机分为TGF组、Pilo组和正常对照组(Control)。建立氯化锂-匹罗卡品癫痫持续状态模型。采用免疫组化方法检测凋亡相关基因Bcl-2、Bax的蛋白表达。结果 (1)SE后24h、48h、72h,TGF组大鼠海马Bax阳性细胞均较Pilo组显著减少(P<0.05);72h最为明显(P<0.01)。HE染色是对各组大鼠海马神经元的形态结构变化的大体观察。(2)SE后24h、48h、72h,TGF组大鼠海马Bcl-2阳性细胞均较Pilo组显著增加(P<0.05);24h最为明显(P<0.01)。结论经鼻(IN)给予TGFβ1可以显著抑制癫痫持续状态诱导的大鼠海马神经元Bax蛋白的表达,上调Bcl-2蛋白表达,从而发挥神经保护作用。

Effects of intranasal transforming growth factor-betal on rat hippocampal Bcl-2 and Bax protein expression after lithium-pilocarpine induced status epilepticus

Objective To investigate the effects of intranasal transforming growth factor-beta1(TGFβ1)on hippocampal Bcl-2 and Bax protein expression after lithium-pilocarpine induced status epilepticus.Method 60 Sprague-Dawley(SD)rats were randomly enrolled into the TGF group,Pilo group and the Control group.The lithium-pilocarpine induced SE was as the SE model.Morphological changes of hippocampal neurons were observed by hematoxylin-eosin(HE)staining.Immunohistochemistry was conducted to detect the expression of Bcl-2 and Bax in hippocampal neurons.Results Intranasal TGFβ1 in TGF group significantly reduced the number of Bax positive cells in Pilo group at 24h(P<0.05),48h(P<0.05)and 72h(P<0.01).Intranasal TGFβ1 in TGF group significantly increased the number of Bcl-2-positive cells in Pilo group at 24h(P<0.01),48h(P<0.05)and 72h(P<0.05).Conclusion Intranasal delivery of transforming growth factor-beta1 can exert potential neuroprotective effect,which may relate to up-regulating Bcl-2 expression and down-regulating Bax expression.