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利用谷氨酸转运体抑制剂制备选择性运动神经元损伤的脊髓片培养模型,在此基础上探讨Ⅱ相酶诱导剂5,6-二氢环戊烯并1,2-二硫杂环戊烯-3-硫酮(CPDT)对运动神经元的保护作用及机制。乳大鼠脊髓片分为正常对照组、THA模型组(100μmol/L苏-羟天冬氨酸;THA)和Ⅱ相酶诱导剂CPDT干预组(15和30μmol/L)。通过免疫组化方法对脊髓腹角α运动神经元进行计数,并利用RT-PCR半定量方法、免疫印迹及酶活性检测等方法,分析各组间醌氧化还原酶1(NQO1)和铁蛋白重链的表达。结果表明CPDT(15或30μmol/L)干预组脊髓腹角的运动神经元数明显增多,与THA模型组相比差异显著(P<0.05,P<0.01),并且经CPDT干预可以有效的诱导NQO1以及铁蛋白重链的表达增加,为下一步在肌萎缩侧索硬化(ALS))动物模型或ALS病人中进行临床干预打下了前期基础。
Preparation of glutamate transporter inhibitor of selective motor neuron injury spinal cord slice culture model, based on this study to phase Ⅱ enzyme inducer 5,6-dihydrocycloheptene 1,2-dithiolane Protective effects and mechanisms of en-3-thione (CPDT) on motor neurons. The spinal cord slices of the rats were divided into normal control group, THA model group (100μmol / L threo - aspartate; THA) and Ⅱ phase enzyme inducer CPDT intervention group (15 and 30μmol / L). Immunohistochemistry was used to count the α-motor neurons in the ventral horn of the spinal cord. The levels of NQO1 and ferritin in each group were analyzed by semi-quantitative RT-PCR, Western blot and enzymatic activity assay. Chain expression. The results showed that the numbers of motor neurons in the ventral horn of spinal cord increased significantly in CPDT (15 or 30 μmol / L) intervention group compared with THA model group (P <0.05, P <0.01), and CPDT intervention could effectively induce NQO1 As well as the increased expression of ferritin heavy chain, laid the foundation for the next step in the clinical intervention in amyotrophic lateral sclerosis (ALS) animal model or ALS patients.