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出 处:《中国康复理论与实践》2005年第12期975-977,i0002,共4页Chinese Journal of Rehabilitation Theory and Practice
基 金:北京市科技新星计划项目(No.953813000);北京市自然科学基金项目(No.7043065)。
摘 要:目的观察LY367385对谷氨酸钠(Glu)及缺糖缺氧(OGD)引起的小鼠大脑皮层神经元损伤的保护作用。方法以细胞乳酸脱氢酶(LDH)漏出、光镜下细胞形态变化为指标,观察培养液中加入Glu或因OGD引起的神经元损伤,以及LY367385的保护作用;用免疫细胞化学和免疫荧光染色法检测神经元代谢型谷氨酸受体1α(mGluR1α)的表达。结果OGD1h或0.1mmol/L的Glu可明显造成神经元损伤,使LDH漏出明显增加(P<0.01);LY367385(50μmol/L)可明显拮抗OGD或Glu引起的神经元损伤,使LDH漏出明显减少(P<0.01);免疫组化检测显示体外培养神经元mGluR1α阳性表达。结论OGD或Glu可能通过激活皮层神经元mGluR1α引起神经元损伤,LY367385通过拮抗mGluR1α保护神经元。Objective To investigate the protective effect of LY367385 on impairment of cultured mouse cerebral cortical neurons induced by sodium glutamate (Glu) or oxygen-glucose deprivation (OGD). Methods Neuron damage induced by Glu or OGD, as well as the action of (S)-(+)-a-amino-4-carboxy-2-methylbenzeneacetic acid (LY367385) were measured by determining the leakage of 1αctate dehydrogenase (LDH) from neurons. Immunocytochemistry and immunofluorescent methods were used to detect the expression of anti-mGluR1α. Morphological observation of primary cortical neurons was performed by phase contrast microscope. Resuits Following the exposure to 0.1 mmol/L Glu for 1 h or OGD for 1 h, LDH leakage from neurons obviously increased ( P〈0.01). 50 mmol/L LY367385, when co-incubated with Glu or OGD, markedly reduced the LDH leakage ( P〈0.01). The 24-h leakage of LDH was increased from cells exposed to 0. 1 mmol/L Glu for 15 min. Pre- and post-treatment with LY367385 (50 mmol/L) decreased the leakage of LDH. The cultured neurons expressed mGluR1α. Conclusion LY367385 has protective effect on neurons damaged by Glu or OGD. It may be re1αted to antagonizing mGluR1α.
关 键 词:神经元 谷氨酸 缺糖缺氧 代谢型谷氨酸受体1α LY367385
分 类 号:R338.1[医药卫生—人体生理学]
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