摘要
目的探讨碱性成纤维细胞生长因子(bFGF)对脑组织缺血再灌注神经元NF-κB的调节作用及机制。方法30只Wista大鼠随机分为Sham组、缺血再灌注组(I/R组)和bFGF组。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2h再灌注损伤24h,采用TUNEL法、免疫组化检测海马及皮质内神经元凋亡和NF-κB的表达。结果sham组海马及皮质偶见凋亡细胞,NF-κBp65在细胞核内无表达,在胞浆内极少表达;I/R组海马及皮质神经元凋亡增加,NF-κBp65在细胞内有所表达,皮质及海马NF-κBp65的表达明显高于sham组。bFGF组大脑皮质及海马NF-κBp65的表达较I/R组明显增多。结论bFGF显著减少缺血神经元凋亡,上调脑缺血诱导的NF-κB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 NF-κB in hippocampus and cortex after cerebral ischemia and reperfusion in rats, explore the regulative effects and mechanism of basic fibroblast growth factor (bFGF)to NF-κB on brain tissue. Methods The model of middle cerebral arteries occlusion (MCAO) were performed with intraluminal filament blockade.the expression of NF-κB and apoptosis cell in hippoeampus and cortex was detected with immunohistochemical method,TUNEL method. Results No apoptotic cells were observed in sham-operation group, The expression of NF-κB in the cortex and hippocampus tissue of rats was at low level in the sham-operation group. In ischemia-reperfusion group apoptotie 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 NF-κB was increased in the model group, The expression of NF-κB 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 NF-κB in ischemic neurons.
出处
《解剖学研究》
CAS
2009年第1期1-4,F0003,共5页
Anatomy Research
基金
辽宁省教育厅科学研究计划项目(05L442)
关键词
脑缺血
碱性成纤维细胞生长因子
NF—κB
海马
凋亡
Cerebral ischemia
Basic fibroblast growth factor (bFGF)
Nuclear factor KB (NF-κB)
Hippocampus
Apoptosis