• <rp id="hvkkj"><menuitem id="hvkkj"></menuitem></rp>

    1. <bdo id="hvkkj"></bdo>
      <b id="hvkkj"><small id="hvkkj"></small></b>

    2. <tt id="hvkkj"></tt>

      1. 當前位置:首頁 > 智慧健康列表 > 認知神經科學與技術 > 詳細信息
        Nec-1 抑制缺氧缺糖誘導的神經元necroptosis 的信號機制
        來源: | 作者: | 發布時間:2013-11-12 9:12:09

        Nec-1 抑制缺氧缺糖誘導的神經元necroptosis 的信號機制
        榮加國,張慧靈
        基金項目:國家自然科學基金項目(30973510)及教育部留學回國人員基金項(K513400110)
        作者簡介:榮加國(1987- ),男,碩士研究生,研究方向:腦血管病藥理學
        通信聯系人:張慧靈(1965- ),女,教授,博導,研究方向:腦血管病藥理學.

         (蘇州大學藥學院藥理系,蘇州,215123)
        摘要:目的:觀察缺氧缺糖誘導的皮層神經元的necroptosis(壞死性凋亡),探究Nec-1 通過抑制RIP1K-自噬-溶酶體信號通路保護缺氧缺糖誘導的神經元necroptosis。方法:原代培養大鼠皮層神經元,采用氧糖剝奪(oxygen-glucose deprivation, OGD)方法建立缺氧缺糖細胞模型。光鏡法觀察OGD 誘導的神經元細胞形態學變化;LDH 法檢測OGD 誘導的神經元乳酸脫氫酶(LDH) 漏出率;Western blot 法檢測Nec-1 對RIP1K-自噬-溶酶體信號通路相關蛋白的表達的影響。結果:在OGD 誘導的神經元損傷模型中,Nec-1 可明顯改善細胞形態,增加細胞數目,降低LDH 漏出率。RIP1K-自噬-溶酶體信號通路相關蛋白RIP1K、LC3、active-Cathepsin B、active-Cathepsin L 表達上調 ,Nec-1 可減少OGD 誘導的神經元中RIP1K、LC3、active-Cathepsin B、active-Cathepsin L 蛋白的表達。結論:Nec-1 對缺氧缺糖誘導的神經元的necroptosis 的保護作用通過抑制RIP1K-自噬-溶酶體信號通路。
        關鍵詞:necroptosis;Nec-1;RIP1K;神經元;OGD
        中圖分類號: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

        奇米色8888