高葡萄糖通过氧化应激介导的 NF-κB 和 MAPK 通路激活诱导 HepG2 细胞中的炎症反应。
High glucose induces inflammatory responses in HepG2 cells via the oxidative stress-mediated activation of NF-κB, and MAPK pathways in HepG2 cells.
机构信息
a Department of Biochemistry, Faculty of Medicine , Tehran University of Medical Sciences , Tehran , Iran.
b Recombinant Protein Laboratory, Department of Biochemistry , Shiraz University of Medical Sciences , Shiraz , Iran.
出版信息
Arch Physiol Biochem. 2018 Dec;124(5):468-474. doi: 10.1080/13813455.2018.1427764. Epub 2018 Jan 24.
OBJECTIVE
The aim of this study was to investigate the effects of high glucose (HG) on inflammation in HepG2 cells.
METHODS
The molecular mechanisms linking HG to inflammation was assessed in HepG2 cells exposed to HG (33 mM).
RESULTS
The results showed that HG significantly enhanced TNF-α, IL-6 and PAI-1 expression in HepG2 cells. Increased expression of cytokines was accompanied by enhanced phosphorylation of JNK, P38, ERK and IKKα/IKKβ. In addition, JNK, ERK, P38 and NF-kB inhibitors could significantly attenuate HG-induced expression of TNF-α, IL-6 and PAI-1. Furthermore, HG could promote the generation of reactive oxygen species (ROS), while N-acetyl cysteine, a ROS scavenger, had an inhibitory effect on the expression of TNF-α, IL-6 and PAI-1 in HG-treated cells.
CONCLUSIONS
Our results indicated that HG-induced inflammation is mediated through the generation of ROS and activation of the MAPKs and NF-kB signalling pathways in HepG2 cells.
目的
本研究旨在探讨高糖（HG）对 HepG2 细胞炎症的影响。
方法
评估了暴露于 HG（33mM）的 HepG2 细胞中，将 HG 与炎症联系起来的分子机制。
结果
结果表明，HG 可显著增强 HepG2 细胞中 TNF-α、IL-6 和 PAI-1 的表达。细胞因子表达增加伴随着 JNK、P38、ERK 和 IKKα/IKKβ磷酸化的增强。此外，JNK、ERK、P38 和 NF-κB 抑制剂可显著减弱 HG 诱导的 TNF-α、IL-6 和 PAI-1 的表达。此外，HG 可促进活性氧（ROS）的产生，而 ROS 清除剂 N-乙酰半胱氨酸对 HG 处理细胞中 TNF-α、IL-6 和 PAI-1 的表达具有抑制作用。
结论
我们的结果表明，HG 诱导的炎症是通过 HepG2 细胞中 ROS 的产生和 MAPKs 和 NF-κB 信号通路的激活介导的。
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