|
KMID : 0624620200530060317
|
|
BMB Reports
2020 Volume.53 No. 6 p.317 ~ p.322
|
|
|
GPx7 ameliorates non-alcoholic steatohepatitis by regulating oxidative stress
|
|
Kim Hyeon-Ju
Lee Yo-Seob
Fang Sungsoon
Kim Won
Kim Hyo-Jung
Kim Jae-Woo
|
|
|
Abstract
|
|
|
|
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases. NAFLD can further progress to irreversible liver failure such as non-alcoholic steatohepatitis (NASH) fibrosis and cirrhosis. However, specific regulator of NASHfibrosis has yet to be established. Here, we found that glutathione peroxidase 7 (GPx7) was markedly expressed in NASH fibrosis. Although GPx7 is an antioxidant enzyme protecting other organs, whether GPx7 plays a role in NASH fibrosis has yet to be studied. We found that knockdown of GPx7 in transforming growth factor-β (TGF-β) and free fatty acids (FFA)- treated LX-2 cells elevated the expression of pro-fibrotic and pro-inflammatory genes and collagen synthesis. Consistently, GPx7 overexpression in LX-2 cells led to the suppression of ROS production and reduced the expression of pro-fibrotic and pro-inflammatory genes. Further, NASH fibrosis induced by choline-deficient amino acid defined, high fat diet (CDAHFD) feeding was significantly accelerated by knockdown of GPx7, as evidenced by up-regulated liver fibrosis and inflammation compared with CDAHFD control mice. Collectively, these results suggest that GPx7 might be a novel therapeutic target to prevent the progression and development of NAFLD.
|
|
|
KEYWORD
|
|
|
Gene therapy, GPx7, NAFLD, NASH, Oxidative stress
|
|
|
FullTexts / Linksout information
|
|
|
|
|
Listed journal information
|
|
  
|