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

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-alpha, IL-6 and PAI-1 expression in HepG2 cells. Increased expression of cytokines was accompanied by enhanced phosphorylation of JNK, P38, ERK and IKK alpha/IKK beta. In addition, JNK, ERK, P38 and NF-kB inhibitors could significantly attenuate HG-induced expression of TNF-alpha, 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-alpha, 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.