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

Effects of intranasal transforming growth factor-beta1 on rat hippocampal Bcl-2 and Bax protein expression after lithium-pilocarpine induced status epilepticus

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。

Objective To investigate the effects of intranasal transforming growth factor-betal （TGFβ1）on hipp- ocampal Bcl-2 and Bax protein expression after lithium-pilocarpine induced status epilepticus. Method 60 Sprague-Daw- ley（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 hippoeampal neurons. Results In- tranasal 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 Intranasaldeliveryoftransforminggrowth faetor-betal can exert potential neuroprotective effect,which may relate to up-regulating Bcl-2 expression and down-regula- ting Bax expression.