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High Glucose Induces Inflammatory Responses in Hepg2 Cells Via the Oxidative Stress-Mediated Activation of Nf-Κb, and Mapk Pathways in Hepg2 Cells Publisher Pubmed



Panahi G1 ; Pasalar P1 ; Zare M2 ; Rizzuto R3 ; Meshkani R1
Authors
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Authors Affiliations
  1. 1. Department of Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Recombinant Protein Laboratory, Department of Biochemistry, Shiraz University of Medical Sciences, Shiraz, Iran
  3. 3. Department of Biomedical Sciences, University of Padova, Padua, Italy

Source: Archives of Physiology and Biochemistry Published:2018


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. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.
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