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作 者:黄俊杰[1] 王彩冰[1] 黄丽娟[1] 何显教[1] 黄彦峰[1] 赵善民[1] 李倩茗[2] 李佳荃[2]
机构地区:[1]右江民族医学院应用生理研究室,广西百色533000 [2]广西医科大学,广西南宁530021
出 处:《中风与神经疾病杂志》2011年第7期601-604,共4页Journal of Apoplexy and Nervous Diseases
基 金:广西教育厅科研项目:桂教科研[2007]34号(200707LX136)
摘 要:目的观察改构型酸性成纤维细胞生长因子(maFGF)对D-半乳糖致衰老大鼠脑组织SOD活力、MDA含量和羟自由基含量及神经细胞凋亡的影响,探讨maFGF对慢性衰老大鼠的抗衰老作用。方法选择成年Wistar大鼠48只,采用皮下注射D-半乳糖建立衰老模型,衰老模型成功后随机分为衰老模型组、生理盐水(NS)对照组和maFGF治疗组。另16只不注射D-半乳糖作为正常对照组。各组大鼠到相对应的时间点取出脑组织,测定脑组织中SOD活力、MDA含量和抑制羟自由基能力;TUNEL法测定大鼠大脑皮质神经细胞凋亡数目。结果衰老模型组大鼠脑组织SOD活力显著降低,MDA含量和羟自由基含量升高,皮质神经细胞凋亡数明显增多;经过用maFGF治疗慢性衰老大鼠后脑组织SOD活力显著升高,MDA含量和羟自由基含量均显著降低,皮质神经细胞凋亡数明显减少。结论 maFGF起到降低自由基,提高脑组织的抗氧化能力,减少皮质神经细胞凋亡数量。Objective To study the effects of modified acidic fibroblast growth factor(maFGF)on the superoxide dismutase(SOD),malondialdehyde(MDA),hydroxyl radical(OH.)and neuronal apoptosis in cerebral cortex of subacute aging model rats.Methods The aging model rats was established by injection of D-galactose.Wistar rats were randomly divided into control group,model of aging group,normal saline(NS)and maFGF treatment group.The SOD,MDA and OH.in cerebral cortex were measured and the number of neuronal apoptosis cells were counted under the high power microscope.Results The MDA,OH.and neuronal apoptosis cells in cerebral cortex of aging model rats were significantly increased than those in control group,but the activities of SOD was significantly decreased than those in control group.After maFGF intervention,the MDA,OH.and neuronal apoptosis cells in cerebral cortex were significantly decreased compared with the NS group and model of aging group respectively,but the activities of SOD were significantly increased than those in control group.Conclusion maFGF possess the reliable function of eliminating free radicals in cerebral cortex,increasing the antioxidative ability of brain tissue and inhibiting the neuronal apoptosis cell in aging model rats.
关 键 词:改构型酸性成纤维细胞生长因子 衰老 自由基 神经细胞 细胞凋亡
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