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机构地区:[1]暨南大学医学院附属二院神经外科,广东深圳518020
出 处:《中风与神经疾病杂志》2004年第1期33-35,共3页Journal of Apoplexy and Nervous Diseases
基 金:卫生部科学基金资助项目 ( 96 0 1 2 8)
摘 要:目的 研究碱性成纤维细胞生长因子 (b FGF)、血管内皮细胞生长因子 (VEGF)在大鼠创伤脑组织中不同时间的表达及其它们之间的关系 ,从分子水平探讨颅脑损伤后的病理机制 ,为临床治疗脑损伤的新途径提供实验基础。方法 改进 Marm arou大鼠加速弥漫性脑损伤模型 ,制作成弥漫性轴索损伤同时合并局灶性脑挫伤的新的动物模型。 SD雄性大鼠 48只 ,随机分为 8组 ,每组 6只。取挫伤灶周围脑组织免疫组化染色观察 b FGF、VEGF基因表达情况。结果 脑挫伤灶周围脑组织 ,b FGF基因表达在伤后 1h明显增加 ,伤后 12 h达高峰 ;VEGF基因表达伤后逐渐增加 ,2 4h达高峰 ,72 h恢复到对照水平。结论 b FGF、VEGF基因表达与脑损伤密切相关 ,作为生长因子 ,b FGF。Objectiv e To study the expressions and interrelationship between bFGF and VEG F in different brain injuried areas and with the model. To investigate the patho genic mechanism of brain injury at molecular level and explore potential effective treatment for the dysfunction. MethodsUsing the modified Marmarou's rode nt model of impact acceleration diffuse brain injury,48 Spranue-Dawley(SD) rats were randomizly d ivided into eight groups (every group n =6). The immunological positive of bFGF,VEG F were observed in these rats using the method of immunohistochemical stain and histopathological HE staining. ResultsThe expression of bFGF mRNA was increased in the cortices in 1hr postinjury and peaked at 12h in marginal areas of injured focus. The expression of VEGF mRNA was increased following brain injury and peak ed at 24h in marginal areas of focal brain injury,returned down to normal at 7 2h. ConclusionThere is a closer relationship between bFG F,VEGF gene expression and the degree of brain injury. As a neurotrophic factor ,bFGF may contribute to neuroprotective effects against injury and repairing following brain injury.
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