NOX3 产生的活性氧通过 JNK 途径促进 TNF-α诱导的肝细胞糖原水平降低。
NOX3-derived reactive oxygen species promote TNF-alpha-induced reductions in hepatocyte glycogen levels via a JNK pathway.
机构信息
Graduate School of Peking Union Medical College and Chinese Academy of Medical Sciences, The Key Laboratory of Geriatrics, Beijing Hospital & Beijing Institute of Geriatrics, Ministry of Health, Beijing 100730, China.
出版信息
FEBS Lett. 2010 Mar 5;584(5):995-1000. doi: 10.1016/j.febslet.2010.01.044. Epub 2010 Jan 25.
TNF-alpha-induced insulin resistance is associated with generation of reactive oxygen species (ROS). This study aims at defining the link between ROS production and hepatic insulin resistance. Treatment with TNF-alpha increased ROS generation through activating NADPH oxidase 3 (NOX3) in HepG2 hepatocytes. Down-regulation of NOX3 using siRNA prevented TNF-alpha-induced decrease of cellular glycogen. In the cells treated with TNF-alpha, there were NOX3-dependent activation of JNK, inhibition of IRS1 and phosphorylation of AKT/PKB and GSK. In conclusion, the effects of TNF-alpha on hepatic insulin resistance appear to be, at least in part, mediated by NOX3-derived ROS through a JNK pathway.
肿瘤坏死因子-α诱导的胰岛素抵抗与活性氧（ROS）的产生有关。本研究旨在确定 ROS 产生与肝胰岛素抵抗之间的联系。TNF-α 处理通过激活 HepG2 肝细胞中的 NADPH 氧化酶 3（NOX3）增加 ROS 的产生。用 siRNA 下调 NOX3 可防止 TNF-α诱导的细胞糖原减少。在 TNF-α处理的细胞中，NOX3 依赖性 JNK 的激活、IRS1 的抑制以及 AKT/PKB 和 GSK 的磷酸化。总之，TNF-α对肝胰岛素抵抗的影响似乎至少部分是由 NOX3 衍生的 ROS 通过 JNK 途径介导的。
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