新生鼠缺氧缺血性脑损伤凋亡基因的变化及神经节苷酯的治疗作用

【目的】探讨新生大鼠缺氧缺血性脑损伤(hypoxic-ischemia brain damage，HIBD)后Bcl-2、Bax基因表达与细胞凋亡的关系及神经节苷酯(gangliosides，GM1)对其的影响。【方法】建立新生鼠HIBD动物模型，用TUNEL法和免疫组化法观察缺氧缺血和GMI干预后不同时间点细胞凋亡情况及凋亡基因Bcl-2、Bax的变化。【结果】缺氧缺血组随时间延长脑组织中Bcl-2、Bax的表达增加，Bcl-2／Bax的比值下降，同时凋亡细胞数增加，表明Bcl-2、Bax两者比值的降低促进凋亡的发生。GM1干预组Bcl-2表达增加显著，降低了Bax的表达，凋亡细胞减少。【结论】GM1可能通过改变凋亡基因的表达而抑制神经细胞的凋亡过程。

Study on the change of apoptotic genes and treatment effect of GM1 in hypoxic ischemic brain damage of neonatal rats

[Objective] To discuss the relationship between expression of Bcl-2,Bax and apoptosis of neonatal rats after cerebral hypoxic-ischemia and effects of gangliosides (GM1) on them. [Method] An animal model of neonatal hypoxic-ischemia brain damage was established. Terminal-deoxynucleotidy transferase mediated nick end labeling (TUNEL)and immunohistochemical were used to detecte apoptosis and Bcl-2,Bax in different time. [Results] A shift in ratio of Bcl-2 to Bax might contribute to neuronal apoptosis after HI. Overexpression Of Bcl-2 protected the cell from apoptosis,but Bax might be functioned as the cell death effectoiver protein. The study showed that immunostaining positive cells of Bcl-2 ptotein was increased while the Bax protein were decreased with the treatment of GM1 after HI. GM1 decreased the apoptosis of cerebral cells. [Conclusion] GM1 may decrease the apoptosis by having an effect on Bcl-2 and Bax.