Bax、NOS在NMDA诱导的兴奋性神经毒中的表达变化

Expression of Bax and NOS in neurons received excitatory neurotoxicity induced by NMDA

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 explore the effects of nitric oxide synthase （NOS） and Bax on excitatory neurotoxicity induced by NMDA and it＇s possible mechanism. Methods Cortical neurons from newborn SD rat were primarily cultured. Purity of cells was assessed by immtmofluorescence techniques. Neurons were divided randomly into 3 groups： normal group, NMDA group and L-NAME group. NO concentration in neurons of each group was detected by NO detection kit, while ELISA was employed to explore the expression of NOS, western blot was used to detect expression of Bax. Results Immunofluorescence test showed that most cells were NSE positive. NO concentration, NOS and Bax expression in L-NAME group were higher than that in normal group, but lower than that in NMDA group. Conclusions NO toxicity play an important role in neuronal apoptosis induced by NMDA, which may be related with up-regulation of Bax expression.