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Nec-1 抑制缺氧缺糖诱导的神经元necroptosis 的信号

  Nec-1 抑制缺氧缺糖诱导的神经元necroptosis 的信号机制

  荣加国,张慧灵

  基金项目:国家自然科学基金项目(30973510)及教育部留学回国人员基金项(K513400110)

  作者简介:荣加国(1987- ),男,硕士研究生,研究方向:脑血管病药理学

  通信联系人:张慧灵(1965- ),女,教授,博导,研究方向:脑血管病药理学.

  (苏州大学药学院药理系,苏州,215123)

  摘要:目的:观察缺氧缺糖诱导的皮层神经元的necroptosis(坏死性凋亡),探究Nec-1 通过抑制RIP1K-自噬-溶酶体信号通路保护缺氧缺糖诱导的神经元necroptosis。方法:原代培养大鼠皮层神经元,采用氧糖剥夺(oxygen-glucose deprivation, OGD)方法建立缺氧缺糖细胞模型。光镜法观察OGD 诱导的神经元细胞形态学变化;LDH 法检测OGD 诱导的神经元乳酸脱氢酶(LDH) 漏出率;Western blot 法检测Nec-1 对RIP1K-自噬-溶酶体信号通路相关蛋白的表达的影响。结果:在OGD 诱导的神经元损伤模型中,Nec-1 可明显改善细胞形态,增加细胞数目,降低LDH 漏出率。RIP1K-自噬-溶酶体信号通路相关蛋白RIP1K、LC3、active-Cathepsin B、active-Cathepsin L 表达上调 ,Nec-1 可减少OGD 诱导的神经元中RIP1K、LC3、active-Cathepsin B、active-Cathepsin L 蛋白的表达。结论:Nec-1 对缺氧缺糖诱导的神经元的necroptosis 的保护作用通过抑制RIP1K-自噬-溶酶体信号通路。

  关键词:necroptosis;Nec-1;RIP1K;神经元;OGD

  中图分类号:R966

  the protection of Nec-1 by inhibiting oxygen-glucose deprivation induced neuronal necroptosis signaling mechanism

  RONG Jiaguo, ZHANG Huiling

  (Department of Pharmacology and Laboratory of Cerebrovascular Pharmacology, College of Pharmaceutical Science, Soochow University, Suzhou 215123)

  Abstract: Objective: To observe the cortex neuronal necroptosis induced by oxygen-glucose deprivation (OGD) and the protection of Nec-1 on OGD-induced neuronal necroptosis by inhibiting RIP1K-autophagic-lysosomal signaling pathway. Methods: Primary rat cortex neurons were cultured,the neurons were exposed to paradigm of ischemic insult by using an OGD device.The morphological changes of neurons induced by OGD were observed by light microscope, cell death was determined by a LDH assay. The effect of Nec-1 on the signaling pathway of RIP1K-autophagic-lysosomal related proteins RIP1K, LC3,active-Cathepsin B, active-Cathepsin L were assessed by western blot analysis.Results:In the OGD-induced neuronal injury model, Nec-1 treatment significantly improved the morphology of neurons, incresed the number of neurons and decreased the LDH leakage. Western blot analysis showed that OGD treatment up-regulated the protein levels of RIP1K-autophagic-lysosomal related proteins RIP1K, LC3, active-Cathepsin B, active-Cathepsin L. Nec-1 treatment decreased the expression of RIP1K, LC3, active-Cathepsin B, active-Cathepsin L.Conclusion: The protective effects of Nec-1 on OGD-induced neuronal necroptosis is associated with inhibiting RIP1K-autophagic-lysosomal signaling pathway.

  Key words: necroptosis; Nec-1;RIP1K ;neuron; OGD

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