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      當前位置:首頁 > 智慧健康列表 > 微循環研究 > 詳細信息
      Atg5 通過激活cathepsins-caspase 信號通路參與缺氧缺糖誘導的小鼠胚胎成纖維細胞的凋亡
      來源: | 作者: | 發布時間:2013-11-12 11:33:42

      Atg5 通過激活cathepsins-caspase 信號通路參與缺氧缺糖誘導的小鼠胚胎成纖維細胞的凋亡
      榮加國,倪勇,陳潔茹,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:在Atg5-/-小鼠胚胎成纖維細胞上,觀察Atg5 是否通過激活cathepsins-caspase信號通路參與缺糖缺氧誘導的小鼠胚胎成纖維細胞的凋亡。方法: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
      MEFs 細胞形態學變化; LDH 法檢測OGD 誘導的MEFs 乳酸脫氫酶(LDH) 漏出率;Westernblot 法檢測cathepsins-caspase 信號通路相關蛋白的表達。結果:在OGD 誘導的MEFs 損傷模型中,與野生型小鼠胚胎成纖維細胞(WT MEFs) 相比,Atg5-/- MEFs 的細胞形態明顯改善,細胞數目顯著增加,LDH 漏出率下降。Active-cathepsin B、active-cathepsin L、tBid、active-caspase 3 的蛋白水平下調, 線粒體Cyt-c 上調和細胞漿Cyt-c 下調。結論:Atg5 參與OGD 誘導的MEFs 細胞凋亡, 其機制與抑制cathepsins-caspase 信號通路的激活有關。
      關鍵詞:Atg5; MEFs; OGD; 細胞凋亡; cathepsins; caspase 3
      中圖分類號:R966
      Atg5 is involved in the mouse embryo fibroblasts apoptosis via activation of the cathepsins-caspase signaling pathway
      RONG Jiaguo, NI Yong, CHEN Jieru, ZHANG Huiling
      (Department of Pharmacology and Laboratory of Cerebrovascular Pharmacology, College of Pharmaceutical Science, Soochow University, Suzhou 215123)
      Abstract: Objective: To investigate the role of Atg5 in OGD-induced apoptosis and its activation of cathepsins-caspase signaling pathway in Atg5-deficient mouse embryo fibroblasts (MEFs).Methods: MEFs were exposed to oxygen-glucose deprivation (OGD). The morphological changes of the MEFs induced by OGD were observed by light microscope, cell death was determined b y a LDH assay. The cathepsins-caspase signaling pathway related proteins were detected by western
      blot analysis. Results: In the OGD-induced MEFs injury model, compared with wild type (WT) MEFs, Atg5-deficient significantly improved the morphology of MEFs, incresed the number of MEFs and decreased the LDH leakage. Western blot analysis showed that OGD treatment induced a decrease in active-cathepsin B and L, tBid, active-caspase 3 and cytoplastic Cyt-c, and an increase in mitochondrial Cyt-c. Conclusion: Atg5-deficient protects MEFs against OGD-induced apoptosis, and its mechanisms is associated with inhibition of cathepsins-caspase signaling pathway.
      Key words: Atg5; MEFs; OGD; apoptosis; cathepsins; caspase 3

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