High glucose induces inflammatory responses in HepG2 cells via the oxidative stress-mediated activation of NF-κB, and MAPK pathways in HepG2 cells.

High glucose induces inflammatory responses in HepG2 cells via the oxidative stress-mediated activation of NF-κB, and MAPK pathways in HepG2 cells.

Arch Physiol Biochem. 2018 Jan 24;:1-7

Authors: Panahi G, Pasalar P, Zare M, Rizzuto R, Meshkani R

Abstract
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.

PMID: 29364751 [PubMed - as supplied by publisher]

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