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目的探讨一氧化氮合酶(nitric oxide synthase,NOS)及Bax在N-甲基-D-天(门)冬氨酸(N-Methyl-D-Asparate,NMDA)诱导的兴奋性神经毒中的作用及其可能的作用机制。方法原代培养SD新生大鼠皮层神经元,利用免疫荧光方法进行细胞纯度鉴定。神经元细胞随机分为正常组、NMDA组、NG-Nitro-L-arginine Methyl Este(r L-NAME)组,分别采用NO浓度测定、ELISA及Weastern blotting检测各组细胞中NO浓度、NOS的表达及Bax的表达。结果免疫荧光大多数细胞为NSE阳性细胞,L-NAME组中NO浓度、NOS及Bax的表达均高于正常组而低于NMDA组。结论 NO毒性在NMDA诱导的神经细胞凋亡中起重要的作用,其可能是通过上调Bax的表达发挥作用。
Objective To investigate the effects of nitric oxide synthase (NOS) and excitatory neurotoxicity of Bax induced by N-methyl-D-asparate (NMDA) Role and possible mechanism of action. Methods Primary cortical neurons of neonatal SD rats were cultured and the purity of cells was identified by immunofluorescence. The neuron cells were randomly divided into normal group, NMDA group and NG-Nitro-L-arginine Methyl Este (r L-NAME) group. NO concentration and NOS expression were detected by ELISA and Weastern blotting respectively. And Bax expression. Results Most of the immunofluorescent cells were NSE positive cells. The concentrations of NO, NOS and Bax in L-NAME group were higher than those in normal group and lower than those in NMDA group. Conclusions NO toxicity plays an important role in the apoptosis of neurons induced by NMDA, which may play a role by up-regulating the expression of Bax.