摘要
目的:应用新生大鼠缺氧缺血性脑损伤(HIBD)模型,观察神经生长因子对海马区细胞凋亡及相关蛋白Bcl-2和Bax的影响,探讨其神经保护作用的分子生物学机制.方法:72只大鼠随机分为对照组、HIBD组和NGF治疗组.应用改良RICE法制作大鼠HIBD模型,TUNEL法检测各组动物海马区细胞凋亡数,免疫组化染色观察Bcl-2,Bax蛋白的表达.结果:与假手术组相比,新生大鼠HIBD后海马区存在不同程度的细胞凋亡,Bcl-2表达轻度升高,Bax表达明显升高.与HIBD组比较,NGF治疗后,凋亡细胞减少(P<0.01),Bcl-2蛋白表达升高(P<0.01),Bax表达下降(P<0.01).结论:HIBD后,新生大鼠海马区细胞存在细胞凋亡,NGF治疗增强Bcl-2表达,减少损伤基因Bax表达,抑制细胞凋亡,具有脑保护作用.
AIM: To investigate the effects of nerve growth factor (NGF) on the expression of apoptosis-related proteins (Bcl-2, Bax)in hippocampus of neonatal rats following hypoxicischemic brain damage (HIBD), and its molecular biological mechanism. METHODS: Seventy-two rats were randomly divid- ed into control group, HIBD group and NGF group. The rat mod- els of HIBD were established by modified RICE method. Immuno- histochemistry and TUNEL staining were employed respectively to detect the expressions of Bcl-2 and Bax and the number of apoptotic hippocampal neurons. RESUILTS: More or less apoptotic neurons could be observed in hippocampus in HIBD group and the level of Bcl-2 expression was elevated slightly, while Bax expression was significantly higher than that in control group. After NGF administration, the number of apoptotic neurons was decreased (P〈0.01), Bcl-2 expression increased (P 〈0.01) and Bax expression decreased remarkably ( P 〈 0.01 ) as compared with HIBD group. CONCLUSION: The administration of NGF may increase Bcl-2 expression and decrease Bax expression after HIBD in neonatal rats, thus inhibiting the apoptosis in hippocampus.
出处
《第四军医大学学报》
CAS
北大核心
2007年第16期1485-1487,共3页
Journal of the Fourth Military Medical University
基金
陕西省2004年社会发展科技攻关项目(2004K11-G9)
关键词
神经生长因子
缺氧缺血
脑
脑损伤
海马
凋亡相关蛋白
nerve growth factor
hypoxia-Ischemia, brain
brain injuries
hippocampus
apoptosis-related protein