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作 者:钟建新[1] 范华燕[1] 黄静 何国厚[1] 钟森[2] 余绍祖[3]
机构地区:[1]湖北省十堰市太和医院神经科 [2]十堰市人民医院 [3]武汉大学人民医院神经科
出 处:《卒中与神经疾病》2002年第5期277-280,共4页Stroke and Nervous Diseases
摘 要:目的 了解局灶性脑缺血病灶周围组织碱性成纤维细胞生长因子 (bFGF)mRNA表达水平 ,探讨bFGF在脑缺血病理过程中的作用机制。方法 采用“线栓法”建立SD大鼠大脑中动脉局灶性脑缺血模型 ,运用NorthernBlot杂交技术并结合图像处理对杂交信号密度扫描以反映bFGFmRNA相对水平。结果 缺血 6小时病灶周期组织即出现bFGFmRNA表达增强 ,1天后达到高峰 (P <0 .0 1)。 1周左右降至对照组水平 ,2周后再次呈现表达增高趋势 ,第 3周时与对照组相比增加约 5 0 % (P <0 .0 5 )。结论 局灶性脑缺血可诱发脑内bFGF基因表达 ,它在保护病灶周围神经元、促进细胞增殖和组织修复中可能发挥着重要作用。Objective To investigate whether the gene expression of basic fibroblast growth factor(bFGF) is enhanced or not and its possible role in the pathogenesis following focal cerebral ischemia.Methods We established the focal cerebral ischemia model of mature Sprague Dawley rats, which were underwent permanent intraluminal occlusion of the left middle cerebral artery(MCA),using 3~0 Nylon monofilament suture. At various time points: 6 hour, 1,3 and 5 day, 1,2 and 3 week after left MCA occlusion, animals were sacrificed by rapid decapitation. The bands intensity of Northern Blot hybridization was quantified using a scanning densitometer to compare different blots and the values indicated the level of bFGF.Results The results showed that levels of bFGFmRNA in tissue surrounding the focal cerebral infarct increased at 6 hours, peaked at 1 day ( P < 0.01 ), declined 3 days, returned to sham level at 7 days and gradually increased again at 14 days, nearly 50 percent increase at the point of 21 days( P < 0.05 ).Conclusion The focal cerebral ischemia can induce the expression of bFGFmRNA. Increased bFGF gene expression may play an important role after focal cerebral ischemia, which may be directly correlated with the extent of cell death, tissue repair and neurological recovery.
关 键 词:实验研究 脑缺血 大鼠 碱性成纤维细胞生长因子 基因
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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