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目的探讨二甲基精氨酸二甲基氨基水解酶(DDAH)/一氧化氮合酶(NOS)途径在甲基苯丙胺(METH)神经毒性中发挥的作用及其相关调控机制。方法将20只♂Wistar大鼠,随机分为NS对照组和METH组,分别ip生理盐水或METH15mg.kg-1,bid,用药4 d。采用HE染色光镜观察大鼠脑组织的病理学改变,Western蛋白印迹法检测大鼠纹状体区的DDAH1蛋白表达水平,以紫外分光光度计检测NOS的活性。结果 METH组大鼠脑组织中出现神经元水肿和明显的噬神经细胞现象,与NS组相比,METH组大鼠纹状体区的DDAH 1蛋白表达水平显著性升高(P<0.05),NOS的活性显著性升高(P<0.01)。结论 DDAH/NOS途径可能参与METH引起的大鼠纹状体区的神经损伤。
Objective To investigate the role of dimethylarginine dimethylaminohydrolase (DDAH) / nitric oxide synthase (NOS) pathway in the neurotoxicity of METH and its related regulatory mechanisms. Methods Twenty male Wistar rats were randomly divided into NS control group and METH group, respectively, ip saline or METH15mg.kg-1, bid, medication 4 d. The pathological changes of rat brain were observed by HE staining, the expression of DDAH1 protein in rat striatum was detected by Western blotting, and the activity of NOS was detected by UV spectrophotometer. Results Compared with the NS group, the expression of DDAH 1 protein in the striatum of the METH group was significantly increased (P <0.05), and the neuronal edema and neuropharyngeal edema appeared in the brain tissue of the METH group. NOS activity was significantly increased (P <0.01). Conclusion DDAH / NOS pathway may be involved in the neurotoxicity induced by METH in rat striatum.