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机构地区:[1]南通大学航海医学研究所,江苏南通226001
出 处:《中风与神经疾病杂志》2006年第5期531-534,共4页Journal of Apoplexy and Nervous Diseases
基 金:江苏省高校自然科学研究计划项目(04KJB310113);南通市社会发展科技计划资助项目(S5041)
摘 要:目的探讨银杏内酯B(Ginkgolide B,Gin B)对缺血中的星形胶质细胞的作用及其机制。方法以新生小鼠纯化的星形胶质细胞,通过缺血(1%O2)或经Gin B预处理,观察细胞形态,活力的变化;利用Westernblot分析bystin与磷酸化Bad蛋白(phosphorylated-Bad,p-Bad)表达的变化。结果星形胶质细胞在缺血0.5h或3h后,变成有反应性特征的星形胶质细胞,活性增高,bystin、p-Bad表达均增加;缺血24h后,细胞变稀疏,胞体变小,突起减少;活性降低;bystin、p-Bad表达明显减少甚至消失;经过Gin B(120μmol/L)预处理后再进行缺血24h,细胞形态较直接缺血明显改善,细胞活性与bystin、p-Bad的表达量均增加。结论Gin B对缺血星形胶质细胞具有保护作用,其作用机制与刺激bystin生成以及增加p-Bad表达有关。Objective To observe the effects of Ginkgolide B(Gin B) on ischemic injury on cultured cortical astrocytes and to approach the mechanisms. Methods We studied the effects of ischemic injury with or without the pretreatment of Gin B by MTT assay and morphologic observation. The expression of bystin, phosphorylated-Bad (p-Bad) were measured by Western blot analysis. Results After ischemia for 0.5h or 3h,astrocytes acquired a characteristic‘reactive’morphology and displayed a series of changes including enhancement of cellular viability and up-regulation of bystin and p-Bad. After ischemia for 24h,the cell bodies began to shrink,processes decurtated or even disappeared,viabilities descended and expression of bystin,p-Bad down-regulated,which were blocked by the pretreatment with Gin B (120μmol/L) for 24h. Conclusion There is an anti-ischemic injury effects of pretreatment of Gin B via enhancing the expression of bystin and p-Bad.
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