摘要
目的研究大鼠脑缺血再灌注后对胞外信号调节激酶(extracellular signal-regulated kinase,ERK)表达的影响,探讨碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF)对脑组织缺血再灌注神经元ERK的调节作用及机制。方法应用线栓法制作大鼠局灶性脑缺血再灌注模型,大脑中动脉阻塞2 h再灌注损伤24 h,采用TUNEL法、免疫组化检测海马及皮质内神经元凋亡和ERK的表达。结果 sham组鼠海马及大脑皮质偶见凋亡细胞,大脑皮质及海马神经元内少见ERK免疫反应阳性细胞;I/R组鼠海马及皮质神经元凋亡增加,缺血再灌注损伤后大脑皮质及海马神经元内ERK阳性表达明显高于假手组;bFGF组鼠海马及皮质神经元凋亡减少,皮质及海马神经元内ERK表达较I/R组明显增加。结论 bFGF显著减少缺血神经元凋亡,上调脑缺血诱导的ERK表达,对脑缺血再灌注海马及皮质神经元的具有保护作用。
Objective To investigate the expression of ERK in hippocampus and cortex after cerebral ischemia and reperfusion in rats,explore the regulative effects and mechanism of basic fibroblast growth factor（bFGF）to ERK on brain tissue.Methods The model of middle cerebral arteries occlusion（MCAO） were performed with intraluminal filament blockade.The expression of ERK and apoptosis cell in hippocampus and cortex were detected with immunohistochemical method and TUNEL method.Results No apoptotic cells were observed in sham-operation group,the expression of ERK in the cortex and hippocampus tissue of rats was at low level in the sham-operation group.In ischemia-reperfusion group apoptotic neurons in ischemic region of cortex and hippocampus enhanced.The decrease of apoptotic neurons in ischemic region of cortex and hippocampus were seen in bFGF treatment group.The expression of ERK was increased in the model group.The expression of ERK in the cortex and hippocampus tissue of rats was markably increased in the treatment group than in the model group.Conclusion The results indicate that bFGF depress cell apoptosis,participate in the regulation of expression of ERK in ischemic neurons.
出处
《解剖学研究》
CAS
2011年第2期81-84,88,共5页
Anatomy Research
基金
辽宁省教育厅科学研究计划项目(L2010546)
