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首页|氯化钆通过激活Akt通路促进Huh7细胞中FoxO1的磷酸化

氯化钆通过激活Akt通路促进Huh7细胞中FoxO1的磷酸化

Gadolinium chloride promoted phosphorylation of FoxO1 by activating Akt pathway in HuH7 cells

中文摘要英文摘要

目的:Akt/FoxO1信号通路是肝细胞中重要的信号转导途径,肝细胞众多功能的正常发挥不可缺少。氯化钆是一种稀土化合物,已经有文献报道,在NIH3T3细胞中,氯化钆能激活Akt信号通路。本文旨在探讨氯化钆对人肝癌细胞系HuH7细胞中Akt通路的作用效果,以及对FoxO1磷酸化水平的影响。方法:体外培养的HuH7细胞,加入氯化钆共孵育48小时后,提取HuH7细胞的蛋白裂解液,用聚丙烯酰胺凝胶电泳结合蛋白免疫印迹分析的方法检测总Akt、磷酸化Akt、总FoxO1及磷酸化FoxO1的蛋白水平。利用Akt通路的特异阻断剂LY294002对Akt磷酸化抑制后,再检测氯化钆对细胞中FoxO1磷酸化的改变。结果:加入氯化钆后,HuH7细胞中的总Akt水平没有显著改变,但磷酸化Akt的水平明显增高。同时,FoxO1的磷酸化水平也增强。而用抑制剂特异阻断了Akt通路后,氯化钆对FoxO1磷酸化的促进效果减弱。结论:HuH7细胞中,氯化钆能通过激活Akt信号通路而促进FoxO1的磷酸化。

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.

陈园园、王倩

基础医学生物化学分子生物学

医学细胞生物学氯化钆ktFoxO1

medical cell biologygadolinium chlorideAktFoxO1

陈园园,王倩.氯化钆通过激活Akt通路促进Huh7细胞中FoxO1的磷酸化[EB/OL].(2014-02-20)[2025-05-05].http://www.paper.edu.cn/releasepaper/content/201402-321.点此复制

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