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作 者:谈冶雄[1,2] 李万亥[1,2] 陶学斌 姜远英[1,2] 陈卫平
机构地区:[1]第二军医大学药学院中西药研究室 [2]第二军医大学药学院药理学教研室
出 处:《第二军医大学学报》1998年第1期39-41,共3页Academic Journal of Second Military Medical University
摘 要:目的:研究乙基4-(3-氧-1,2-苯并异硒吡咯-2-基)-α-甲基-苯乙酸盐(EOBMB)对培养神经元缺氧损伤的保护作用及机制。方法:培养大鼠皮质神经元通以95%N2+5%CO2造成缺氧模型;体外产生的超氧阴离子和羟自由基刺激培养神经元;测定培养上清乳酸脱氢酶(LDH)活性和硫代巴比妥酸反应活性物质(TBARS)含量;观察EOBMB对超氧阴离子和羟自由基特征显色反应的影响;测定谷胱甘肽过氧化物酶(GSH-Px)拟似活性。结果:EOBMB能抑制缺氧和自由基诱发的培养神经元的LDH释放和TBARS含量的增加。体外无直接灭活超氧阴离子和羟自由基的活性,但表现一定的GSH-Px活性。结论:EOBMB对神经元缺氧损伤具有保护作用,作用机制主要通过发挥GSH-Px活性,抑制自由基的脂质过氧化。Objective:To study the protective effect of ethyl- 4-(3-oxo-1,2-benzisoselenazol-2-yl)-α-methyl-benzeneacetate (EOBMB) on anoxia-induced injury to cultured rat cortical neurons. [WTHZ] Methods: [WTBZ] Cultured cortical neurons were placed under 95% N_2 and 5% CO_2 as an anoxia model. O_2 produced by hypoxanthine/xanthine oxidase and ·OH produced by vitamin C/CuSO4 stimulated cultured neurons. LDH activity and TBARS content were assayed spectrophotometrically. Effect of EOBMB on color reaction of O_2 and ·OH was evaluated. GSHPx activity of EOBMB was determined. Results: EOBMB depressed LDH efflux and increase of TBARS content in cultured neurons induced by anoxia and free radicals. In vitro, EOBMB had no direct inactive activity on O_2 and · OH while showed certain GSHPx activity. Conclusion: EOBMB has a protective effect on neuron damage indued by anoxia, which derives from depressing lipid peroxidation damage induced by free radicals as a GSHPx mimicry.
分 类 号:R743.310.5[医药卫生—神经病学与精神病学]
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