摘要
目的:探讨新生大鼠缺氧缺血性脑损伤(HIBD)后海马CA1区脑红蛋白(Ngb)及凋亡相关蛋白Bcl-2、Bax的变化规律及其相关性。方法:选用60只新生7日龄Wistar大鼠,随机分为三组:sham组(n=6),正常对照组(n=6)和HIBD组(n=48)。HIBD组新生大鼠建立HIBD模型,分别于HIBD后3h、6h、12h、24h、48h、72h、7d、14d取材,应用免疫组织化学染色方法检测各组海马CA1区Ngb及Bcl-2、Bax的表达变化情况。结果:(1)与sham组相比,HIBD组Ngb阳性细胞数于缺氧缺血后3h开始下降,但差异无统计学意义;6h、12h、24h呈逐渐下降趋势,阳性细胞数量已明显低于sham组;到48h时达最低水平;14d时Ngb阳性细胞数量基本恢复至sham组水平。(2)与sham组相比,HIBD组于缺氧缺血3hBcl-2阳性表达细胞开始显著增多,于12h达到高峰,24h时开始逐渐下降,14d时略高于sham组表达,但差异无统计学意义。(3)与sham组相比,HIBD组Bax蛋白免疫反应阳性细胞数目于缺氧缺血后3h时开始增加,12h时明显增多,于48h达高峰,此后逐渐下降,7d时阳性细胞数基本恢复至sham组水平,14d时未见Bax蛋白的阳性表达。(4)新生大鼠海马CA1区内,Ngb阳性细胞数与Bcl-2阳性细胞数无相关;与凋亡相关蛋白Bax阳性细胞数呈负相关(r=-0.697,P<0.01)。结论:Bcl-2与Bax基因参与了HIBD后神经细胞凋亡的发生;Ngb可能通过抑制促凋亡蛋白Bax的表达,从而减少神经细胞的凋亡,发挥其神经保护作用。
AIM：To study the relationship between the expression of Bcl-2,Bax and neuroglobin（Ngb） protein in neonatal rats hippocampus with hypoxic-ischemic brain damage.METHODS：60 7-day-old Wistar rats were randomly divided into three groups：sham group（n=6）,control group（n=6）,HIBD group（n=48）.The animals in HIBD group were sacrified by decapitation on 3 h,6 h,12 h,24 h,48 h,72 h,7 d,14 d.Rats were used to study histological change and the protein expression for Bcl-2,Bax and Ngb by thionin staining and immunohistochemistry.RESULTS：（1） Compared with sham group and control group,the number of positive cells began decreasing after HIBD for 3 hours,obviously decreased after HIBD for 6,12,24 hours,was the lowest marker after HIBD for 48 hours,then increased,came back the level of sham group after HIBD for 14 d.（2） Compared with sham group and control group,the number of positive cells obviously increased in HIBD groups.After HIBD for 3 hours,the number of positive cells significantly increased,was the highest marker after HIBD for 12 hours,then decreased at 24 h,were higher than that of sham group and control group,but there were no significantly different after HIBD for 14 d.（3） Compared with sham group and control group,the number of positive cells began increasing after HIBD for 3 hours,obviously increased after HIBD for 12 hours,was the highest marker after HIBD for 48 hours,then decreased,came back the level of sham group after HIBD for 7 d.There was no positive cells after HIBD for 14 d.（4） There was no correlation between the number of positive cells which expressed Bcl-2 protein with the number of positive cells which expressed Ngb protein and it’s negative correlation between the number of positive cells which expressed Bax protein with the number of positive cells which expressed Ngb protein（r=-0.697,P〈0.01）.CONCLUSION：The expression of Bcl-2 and Bax gene plays a role in the process of neuronal apoptosis following HIBD.Ngb protein maybe decrease the neuronal apoptosis and play the protective effects by restraining the expression of Bax.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2010年第10期1040-1042,共3页
Chinese Journal of Cellular and Molecular Immunology
