神经生长因子和神经节苷脂对新生鼠缺氧缺血性脑损伤海马神经细胞的保护作用

目的 观察联用神经生长因子(nerve growth factor,NGF)和神经节甘脂(ganglioside GM1)对实验大鼠缺氧缺血性脑损伤的治疗作用,探讨其神经保护的可能机制.方法 120只新生鼠分为假手术组、缺氧缺血性脑损伤(hypoxic-ischemic brain injury,HIBI)组、NGF治疗组、GM1治疗组和NGF GM1治疗组.给药后以HE染色观察各组海马区神经细胞形态变化,免疫组化观察Bcl-2、Bax蛋白表达,TUNEL法观察海马区神经细胞凋亡情况.结果 缺氧缺血后HIBI组海马区病理变化明显,药物干预组上述变化减轻,合用组为著;假手术组海马区Bcl-2表达较弱,HI(缺氧缺血)后该区Bcl-2表达仍弱,Bax表达增强,出现凋亡细胞;药物干预组Bcl-2表达较HIBI组增强,Bax表达较HIBI组减弱(P＜0.01),凋亡细胞减少,合用组最明显.结论 HIBI后Bax蛋白表达增强,细胞凋亡增加.两药联用可上调Bcl-2表达,下调Bax表达,使凋亡细胞减少,这可能是其治疗新生儿缺氧缺血性脑损伤的机制之一.

Protective effect of combined NGF and ganglioside GM1 on hypoxic-ischemic brain injury of newborn rats

Objective To study the therapeutic effect of combined administration of nerve growth factor(NGF)and ganglioside GM_ 1 on the hypoxic-ischemic brain injury(HIBI)rat model and the relevant involving mechanisms.Methods A total of 120 7-day old rats were randomly divided into 5 groups:sham-operation group,HIBI group,NGF group,GM_ 1 group and NGF GM_ 1 group.HE staining,immunohistochemical staining and TUNEL staining were employed respectively to study the morphological changes,bcl-2 and Bax expressions and apoptosis in the hippocampal neuron after treatment.Results Pathological changes were observed in the hippocampal neuron after HIBI.In NGF GM_ 1 group,the level of Bcl-2 expression was increased significantly(P<0.01),while that of Bax and the number of apoptotic cells in the hippocampal region were decreased significantly in comparison to the HIBI group(P<0.01).Conclusion The combined administration of NGF and GM_ 1 may increase Bcl-2 expression and attenuate Bax expression,and thus inhibit the apoptosis in hippocampal region.