Objective:
To investigate the effect of peroxiredoxin1 (Prdx1) on the methionine-choline deficient (MCD)-
induced mice model of non-alcoholic fatty liver disease (NAFLD).
Methods:
Wild type (WT), transgenic Prdx1 over-expressing (TG) and Prdx1 knockout (KO) mice were fed with MCD
diet to construct NAFLD model. General parameters was determined followed by detection with HE staining, oil red O
staining, Immunofluorescence, Immunohistochemistry, qRT-PCR and Western blotting. The activities of MDA, GPX and
SOD were also quantified.
Results:
Compared with WT + MCD group, mice in KO + MCD group showed the decresed final weight, food intake and
the levels of glucose, insulin, total cholesterol and triglyceride, accompanying with the increased FFA, ALT and AST, as
well as the aggravated liver histopathology, which was alleviated in TG + MCD group. Also, mice from KO + MCD
group had increased F4/80 and CD68 positive staining with the upregulation of pro-inflammatory and fibrogenic factors in
liver tissues than those from WT + MCD group, as well as the enhanced MDA and the reduced GPX and SOD, while TG
+ MCD group demonstrated improvements than the WT + MCD group. Nrf-2/HO-1 pathway in liver tissues from
NFALD mice was inhibited, and Prdx1-/-
can further reduce the expression of Nrf-2 and HO-1, while Prdx1 overexpression increased Nrf-2 and HO-1 expression.
Conclusion:
Prdx1 improved oxidative stress, inflammation and fibrosis in liver of NAFLD mice, which may be associate
with the activation of Nrf-2/HO-1 pathway.
FXYD6 overexpression in HBV-related hepatocellular carcinoma with cirrhosis
