mTORC2/SGK1信号通路对ENaC各亚基调控的体外研究

王海霞; 刘振峰

mTORC2/SGK1信号通路对ENaC各亚基调控的体外研究

Regulation of ENaC subunits by mTORC2/SGK1 signaling pathway in vitro

摘要

摘要:
目的： 从体外探讨mTORC2/SGK1信号通路对ENaC各亚基的影响。
方法： 通过培养A549细胞并成功建立急性肺损伤模型，采用ELISA、细胞免疫荧光及蛋白印迹等方法分别检测炎性介质、ENaC各亚基及mTORC、p–Nedd4–2和SGK1（p–SGK1）的表达水平。
结果： 与对照组比较，LPS组ENaC–α、ENaC–β、ENaC–γ的表达均降低，差异有统计学意义（P ＜ 0.05）。LPS组IL–6、IL–8、TNF–α均较对照组增加，差异有统计学意义（P ＜ 0.05）。与对照组比较，LPS组mTORC表达升高，SGK1（p–SGK1）和p–Nedd4–2表达降低（P ＜ 0.05）。
结论： mTORC2/SGK1的信号通路能调节ENaC的表达，炎性介质在急性肺损伤的发生、发展中其重要的作用。

Abstract:
Objective To discuss the influence of mTORC2/SGK1 signaling pathways on ENaC subunits in vitro;
Methods The ALI model was successfully established through the cultivation of A549 cells. The expression levels of inflammatory mediators, ENaC subunits, mTORC, p-Nedd4-2 and SGK1 (p-SGK1） were detected by ELISA, cell immunofluorescence and western blotting.
Results Compared with control group, the expressions of ENaC-α, ENaC-β, ENaC-γ in LPS group were decreased (P ＜ 0.05）. The differences were statistically significant. IL-6, IL-8, TNF-α in LPS group increased compared with those in control group and the differences were statistically significant (P ＜ 0.05）. Compared with the control group, the expression of mTORC was increased and the expressions of SGK1 (p-SGK1） and p-Nedd4-2 were decreased in LPS group (P ＜ 0.05）.
Conclusions mTORC2/SGK1 signaling pathway can regulate the expression of ENaC, and inflammatory mediators play an essential role in the occurrence and development of acute lung injury.

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