Effect of HBx on inflammation and mitochondrial oxidative stress in mouse hepatocytes.

Abstract:

:Hepatitis B virus × protein (HBx) serves an important role in the pathogenesis of the hepatitis B virus infection. Previous studies have reported that the interaction between HBx and hepatocyte mitochondria is an important factor leading to liver cell injury and apoptosis, ultimately inducing the formation of liver cancer. In the present study, a mouse model expressing HBx was constructed using hydrodynamic in vivo transfection based on the interaction between HBx and cytochrome c oxidase (COX) subunit III. The specific mechanism of HBx-induced oxidative stress in mouse hepatocytes and the subsequent effect on mitochondrial function and inflammatory injury was assessed. The results demonstrated that HBx reduced the activity of COX and the expression of superoxide dismutase and upregulated the expression of malondialdehyde, NF-κB and phospho-AKT, thus increasing oxidative stress. In addition, HBx induced an increase in interleukin (IL)-6, IL-1β and IL-18 expression levels, which created an inflammatory microenvironment in the liver, further promoting hepatocyte inflammatory injury. Therefore, it was proposed that HBx may affect hepatocyte mitochondrial respiration by reducing the activity of cytochrome c oxidase, leading to mitochondrial dysfunction and inducing hepatocyte inflammation and injury.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Ling LR,Zheng DH,Zhang ZY,Xie WH,Huang YH,Chen ZX,Wang XZ,Li D

doi

10.3892/ol.2020.11404

subject

Has Abstract

pub_date

2020-04-01 00:00:00

pages

2861-2869

issue

4

eissn

1792-1074

issn

1792-1082

pii

OL-0-0-11404

journal_volume

19

pub_type

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