摘要
为了探讨 bcl- 2基因家族成员 bax,bcl- 2的表达产物 Bax、 Bcl- 2与电针抗缺血脑损伤的关系。本实验采用改良线拴法制备大鼠大脑中动脉 (MCA )阻塞 -再灌注模型 ,并用 TTC及 HE染色观察缺血及电针后梗塞灶的变化 ,用免疫组织化学方法对大鼠局灶性脑缺血组织内 Bax,Bcl- 2免疫阳性细胞的分布及电针对该分布的影响进行观察。发现 :1.行为生理学观察 :电针组大鼠神经缺损 Bederson综合评分明显低于缺血组综合评分 (P<0 .0 5 ) ;2 .TTC染色表明梗塞灶中心位于尾壳核 ,累及大脑皮层 ;HE染色计算缺血组梗塞灶体积为 74.72± 3.6 7m m3,电针组为 5 2 .6 6± 1.81mm3,两组间有显著性差异 (P<0 .0 1) ;3.大鼠 MCA阻塞 30 m in再灌注 48小时后 ,缺血组及电针组梗塞灶中心 (尾壳核 )偶见 Bax及 Bcl- 2免疫阳性细胞 ;缺血组半影区 Bax阳性细胞数量显著增加 (P<0 .0 1)。 Bcl- 2免疫阳性细胞数反应性上调 (P<0 .0 5 ) ;电针组半影区 Bax的表达与缺血组相比下调 (P<0 .0 5 ) ,但仍高于对照组 (P<0 .0 5 ) ;Bcl- 2的表达与缺血组之间无差异显著性。海马 CA1区神经元 Bax,Bcl- 2的表达在各组间均无显著性差异。结果表明电针有抗缺血脑损伤的效应 ,其分子机制之一可能是通过下调半影区 Bax的表达而相对降低 Bax/Bcl-
In order to investigate the relationship between expression of Bax/Bcl 2 and the role of electroacupuncture (EA) after focal cerebral ischemia, the animal model of middle cerebral artery occlusion (MCAO) and immunohistochemical staining methods were used. Meanwhile, the brain section were stained by TTC and HE for surveying area of infarction. The results were found as below: ① Bederson standards grading to determine the symptom of nerve dificient, showed that the mean of Bederson standards of grading in EA group is remarkablely lower than MCAO group ( P <0 05) ② Pathological change of the area of infraction in EA group were lower than MCAO group by HE staining, the infraction volume counted in MCAO group (74 72±3 67 mm 3) is more than MCAO+EA group(52 66±1 81 mm 3) ③ In the core of MACO group, caudoputamen, we barely observe the Bax and Bcl 2 positive neurons, however, in penumbra, we observed an increasing immunoreactivity of Bax and Bcl 2 comparing with sham operated group( P <0 05) In penumbra of MCAO+EA, we observed an decreasing immunoreactivity of Bax comparing with MCAO group ( P <0 05) The result suggested that therapy of EA is effective on focal cerebral ischemic disease, and one of molecular mechanism was EA down regulating the expression of Bax and leaded Bax/Bcl 2 ratio decreased.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2001年第1期27-32,共6页
Chinese Journal of Histochemistry and Cytochemistry
基金
国家自然科学基金资助课题 (No.395 0 0 191)