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      當前位置:首頁 > 智慧健康列表 > 細胞分子生物學 > 詳細信息
      氯化釓通過激活Akt通路促進Huh7細胞中FoxO1的磷酸化
      來源: | 作者: | 發布時間:2014-4-15 14:37:50

       氯化釓通過激活Akt通路促進Huh7細胞中FoxO1的磷酸化
      王倩,陳園園
      基金項目:國家自然科學青年基金(31101011,81271828);高等學校博士學科點專項科研基金(20103234120003);南京醫科大學基礎醫學院青年教師培養基金(09JC002);南京醫科大學科技發展基金項目(09NJMUZ03) 作者簡介:王倩(1980年生),女,現任南京醫科大學副教授,主要從事病毒性肝炎、糖尿病的相關研究 通信聯系人:陳園園(1980年生),女,現任南京醫科大學基礎醫學院生物化學與分子生物學系講師,主要從事糖尿病及并發癥發病與治療的相關機制研究.

      (南京醫科大學基礎醫學院生物化學與分子生物學系,江蘇省人類功能基因組學重點實驗5 室,江蘇省南京市,210029)
      摘要:目的:Akt/FoxO1信號通路是肝細胞中重要的信號轉導途徑,肝細胞眾多功能的正常發揮不可缺少。氯化釓是一種稀土化合物,已經有文獻報道,在NIH3T3細胞中,氯化釓能激活Akt信號通路。本文旨在探討氯化釓對人肝癌細胞系HuH7細胞中Akt通路的作用效果,以及對FoxO1磷酸化水平的影響。方法:體外培養的HuH7細胞,加入氯化釓共孵育48小時后,提取HuH7細胞的蛋白裂解液,用聚丙烯酰胺凝膠電泳結合蛋白免疫印跡分析的方法檢測總Akt、磷酸化Akt、總FoxO1及磷酸化FoxO1的蛋白水平。利用Akt通路的特異阻斷劑LY294002對Akt磷酸化抑制后,再檢測氯化釓對細胞中FoxO1磷酸化的改變。結果:加入氯化釓后,HuH7細胞中的總Akt水平沒有顯著改變,但磷酸化Akt的水平明顯增高。同時,FoxO1的磷酸化水平也增強。而用抑制劑特異阻斷了Akt通路后,氯化釓對FoxO1磷酸化的促進效果減弱。結論:HuH7細胞中,氯化釓能通過激活Akt信號通路而促進FoxO1的磷酸化。
      關鍵詞:醫學細胞生物學;氯化釓;Akt;FoxO1
      中圖分類號:Q257 20
      Gadolinium chloride promoted phosphorylation of FoxO1 by activating Akt pathway in HuH7 cells
      Qian Wang, Chen Yuanyuan
      (Jiangsu Province Key Lab of Human Functional Genomics, Department of Biochemistry and   Molecular Biology, Nanjing Medical University, Nanjing 210029, P.R. China)
      Abstract: Objective: Akt/FoxO1 pathway is one of the most important signal pathways in liver cells. Gadoliniu chloride is a rare earth compound. It has been reported that gadolinium chloride could activate the Akt pathway in NIH3T3 cells. In this paper, the effect of gadolinium chloride on the Akt pathway and phosphorylation of FoxO1 in HuH7 cells was investigated. Methods: Lysis was extracted from the HuH7 cells after incubation with gadolinium chloride, and detected the levels of Akt, phosphorylated Akt, FoxO1 and phosphorylated FoxO1 with western blotting analysis. Then the effect of gadolinium chloride on phosphorylation of FoxO1 was detected after Akt pathway was inhibited by LY294002. Results: The level of total Akt did not change, but the phosphorylation levels of Akt increased greatly under the action of gadolinium chloride, and the same change was observed on phosphorylated FoxO1. And the role of gadolinium chloride decreased greatly after inhibition of Akt pathway. Conclusion: In HuH7 cells, gadolinium chloride could promote the phosphorylation of FoxO1 by activating the Akt pathway.
      Key words: medical cell biology; gadolinium chloride; Akt; FoxO1

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