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作 者:谢赛[1] 董军[1] 余启贵 黄涛[1] 付咏梅[1]
机构地区:[1]暨南大学医学院病理生理学教研室,广东广州510632 [2]美国印第安纳大学医学院微生物和免疫学系,美国印第安纳州46202
出 处:《暨南大学学报(自然科学与医学版)》2010年第4期352-356,共5页Journal of Jinan University(Natural Science & Medicine Edition)
基 金:国家中医药管理局病理生理学重点实验室开发放基金项目(51207029);广东省自然科学基金项目(06105246;9151040701000008);广州市科技计划项目(2007J1-C0041)
摘 要:目的:探讨姜黄素对IL-6损伤的大鼠海马神经元的功能性保护作用及其机制。方法:应用离体脑片记录技术,记录大鼠海马CA1区的兴奋性突触后电位(EPSP),给予Schaffer侧支高频电刺激(HFS)诱发长时程增强(LTP),观察不同药物处理组EPSP起始斜率的变化情况。结果:与对照组相比,IL-6和N-甲基D-天冬氨酸(NM-DA)对大鼠海马脑片的LTP产生明显的抑制作用(P<0.05);而姜黄素可部分拮抗IL-6和NMDA对海马脑片LTP的抑制作用,与模型组相比差异有统计学意义(P<0.05);IL-6、姜黄素和NMDA对大鼠海马神经元的基础突触传递无影响。结论:姜黄素对海马神经元具有功能性保护作用,其机制可能是作用于神经元细胞膜上的NMDA受体,拮抗IL-6引起神经元功能异常。Aim:The present study was performed in vitro on rat brain slices to determine the functional effect of curcumin on IL-6-induced neuronal damage in rat hippocampus,and to study the molecular mechanism of the impact for curcumin on IL-6 neurotoxicity. Methods: In vitro brain slices recording techniques were used to record the excitatory postsynaptic potential(EPSP) of CA1 pyramidal layer of rat hippocampal brain slices.High frequency stimulation(HFS) was given on Schaffer branches to induce long-term potentiation(LTP).The initial slope of EPSP was then measured in the treatments of IL-6 or NMDA with or without curcumin.Results: Compared with the control group incubated only with artificial cerebrospinal fluid(ACSF),IL-6 and NMDA markedly inhibited LTP of hippocampal brain slices of rats(P0.05).The inhibition ofLTP by IL-6 or NMDA was partially but significantly prevented by addition of curcumin(IL-6 versus IL-6 plus curcumin,P0.05;NMDA versus NMDA plus curcumin,P0.05).IL-6,curcumin and NMDA had no effects on basal synaptic transmission of hippocampal slices.Conclusion:Curcumin has a protective role on hippocampal neurons through NMDA receptor on the neuronal omembrane,reversing the damage induced by IL-6.
关 键 词:HIV-1相关痴呆(HAD) 姜黄素 白介素6(IL-6) 长时程增强(LTP) N-甲基-D-天门冬氨酸(NMDA)
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