摘要
目的研究信号分子SH2-Bβ在局灶性脑缺血再灌注大鼠大脑顶叶皮质表达情况为阐明脑缺血的演变的分子机制从而为临床治疗提供理论依据。方法用线栓法阻塞大鼠右侧大脑中动脉制作局灶性脑缺血再灌注模型,动物随机分为假手术组和缺血再灌注组,应用免疫组织化学SABC法和图像分析方法检测大鼠顶叶皮质SH2-Bβ表达情况。结果假手术组右侧顶叶皮质SH2-Bβ有很少的表达,而缺血再灌注组3 h时间点SH2-Bβ在右侧顶叶皮质的平均光密度值比假手术组明显增高,持续到24 h,到48 h时间点开始下降,到72 h已逐渐下降但仍高于假手术组(P<0.05)。结论局灶性脑缺血再灌注大鼠顶叶皮质SH2-Bβ被诱导而表达增高,SH2-Bβ可能参与NGF对缺血神经元的保护作用机制,促进神经元存活和损伤的修复。
Objective To study the expression of the signal molecular-SH2-Bβ in focal cerebral ischemia/ reperfusion （I/R） rats and explore the molecular mechanism of I/R. Methods Focal cerebral I/R model was induced by occlusion of the fight middle cerebral artery using the intraluminal suture method. The male rats were divided into sham group and cerebral I/R group randomly. The expression of SH2-Bβ was detected with immunohistochemistry SABC method and analyzed by image analysis system. Results Positive product of SH2-Bβ in the sham group was barely detected. In contrast, there was a marked increase of the average optical density （AOD） of SH2-Bβ 3 hrs reperfusion following 2 hrs middle cerebral artery occlusion （MCAO） , and this trend continued to 24 hrs reperfusion and began to decrease 48 hrs reperfusion. The average optical density of SH2-Bβ reduced markedly but was still higher in ischemic rats with 72 hrs reperfusion than in sham group （ P 〈 0.05）. Conclusion The overexpression of SH2-Bβ in parietal lobe after focal cerebral I/R indicates that it probably involves in the mechanism of NGF mediated protective role for ischemie neurons.
出处
《解剖科学进展》
CAS
2006年第2期129-131,i0006,共4页
Progress of Anatomical Sciences
基金
辽宁省自然科学基金资助项目(No619019)
