摘要
[目的]探讨神经节苷脂(gangliosides,GM1)对新生大鼠缺氧缺血性脑损伤(hypoxic-ischemicbraindamage,HIBD)的保护作用及其机制,为临床治疗新生儿缺氧缺血性脑病提供依据。[方法]建立新生大鼠HIBD模型,应用HE染色、DNA原位末端标记法(TUNEL)、免疫组化染色与医学图像分析相结合方法观察正常对照组、假手术组、生理盐水组及GM1干预组海马CA1区在缺氧缺血后6、24、72h、7d病理变化、神经细胞凋亡及Bcl-2、Bax蛋白表达。[结果]①缺氧缺血后生理盐水组海马CA1区病理变化明显,GM1干预组上述变化减轻;②正常对照组及假手术组海马CA1区Bcl-2表达较弱,HI后该区Bcl-2表达仍弱,Bax表达增强,出现凋亡细胞,以3d最明显;GM1干预组Bcl-2表达较盐水组增强,Bax表达较盐水处理组减弱(P<0.01),凋亡细胞减少。[结论]HIBD后Bax蛋白表达增强,细胞凋亡增加。GM1可上调Bcl-2表达,下调Bax表达,使凋亡细胞减少,这可能是GM1治疗新生儿缺氧缺血性脑损伤的机制之一。
[Objective] To investigate the protective effect and mechanism of gangliosides(GM1) on the brain of hypoxic-ischemic damage in the newborn rats. [Methods] After the establishment of hypoxic-ischemic brain damage animal model in newborn rats, the pathologic changes, neural cell apoptosis, and the expression of Bcl-2 and Bax were observed in control group, pseudo-operation group, saline group and GM1 affected group at 6, 24, 72 h and 7 d through the techniques of HE staining, in situ end-labeling,immunohistochemical staining and medical image analyzing. [Results] The pathological changes of the hippocampal A1 region in saline group were apparent than those of the GM1 affected group after hypoxic-ischemia. The expression of Bcl-2 in the A1 region were not obvious before and after hypoxic-ischemia in control group and pseudo-operation group, but the expression of Bax increased after hypoxic-ischemia and reached the peak at 3 d. The expression of Bcl-2 in the GM1 affected group was more obvious than that of saline group, but the expression of Bax in the GM1 affected group was less obvious than that of saline group(P<0. 01). [Conclusions] The expression of bax protein increases after hypoxic-ischemic brain damage, GM1 makes Bcl-2 expression increase and decrease the expression of bax. This maybe the possible therapy mechanism of GM1 on the brain after hypoxic-ischemic damage in newborn.
出处
《中国儿童保健杂志》
CAS
2005年第2期131-133,共3页
Chinese Journal of Child Health Care
关键词
神经节苷脂
脑缺氧
脑缺血
凋亡
gangliosides
cerebral ischemia
cerebral hypoxia
apoptosis
