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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c-Myc蛋白表达影响及机制。方法 30只大鼠随机分为假手术组、缺血再灌注组、bFGF组,每组10只;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,采用原位末端标记法(TUNEL)、免疫组织化学法检测海马及顶叶皮质内神经元凋亡和c-Myc蛋白表达。结果假手术组大鼠海马及顶叶皮质偶见凋亡细胞,神经元内少见c-Myc蛋白阳性细胞;缺血再灌注组海马及顶叶皮质神经元凋亡增加,顶叶皮质及海马神经元内c-Myc蛋白表达灰度值为(88.16±2.43),(86.72±1.23),bFGF组神经元凋亡减少,神经元内c-Myc蛋白表达灰度值为(97.61±1.78),(95.35±2.34)。结论 bFGF可减少缺血神经元凋亡,抑制脑缺血诱导的c-Myc蛋白的表达,对脑缺血再灌注海马及顶叶皮质神经元具有保护作用。
Objective To investigate the effect of basic fibroblast growth factor (bFGF) on the expression of c-Myc in cerebral ischemia-reperfusion neurons and its mechanism. Methods Thirty rats were randomly divided into sham-operated group, ischemia-reperfusion group and bFGF group, with 10 rats in each group. The focal cerebral ischemia-reperfusion model was established by thread occlusion. Twenty-four hours after perfusion, TUNEL and c-Myc protein expression in hippocampus and parietal cortex were measured by immunohistochemistry. Results Apoptotic cells and c-Myc positive cells were rare in hippocampus and parietal cortex in sham operation group. Apoptosis of neurons in hippocampus and parietal cortex was increased in ischemia-reperfusion group. The gray value of c-Myc protein expression was (88.16 ± 2.43) and (86.72 ± 1.23) in bFGF group, and decreased in bFGF group. The gray value of c-Myc protein in neurons was (97.61 ± 1.78), ( 95.35 ± 2.34). Conclusion bFGF can reduce the apoptosis of ischemic neurons, inhibit the expression of c-Myc induced by cerebral ischemia, and protect the hippocampus and parietal cortex neurons from cerebral ischemia / reperfusion.