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The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
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Ursolic acid ameliorates CCl4-induced liver fibrosis through the NOXs/ROS pathway

Dakai Gan1, Wang Zhang2, Chenkai Huang2

  • 1Department One of Liver Disease, The Ninth Hospital of Nanchang, Nanchang, People's Republic of China.

Journal of Cellular Physiology
|April 20, 2018
PubMed

Insights

Ursolic acid (UA) reverses liver fibrosis by reducing NADPH oxidases (NOXs) and reactive oxygen species (ROS) in liver cells. This treatment promotes hepatocyte proliferation and hepatic stellate cell apoptosis without impairing host defense.

Area of Science:

  • Hepatology
  • Cell Biology
  • Biochemistry

Background:

  • Liver fibrosis is a dynamic wound-healing process following liver injury.
  • NADPH oxidases (NOXs) and reactive oxygen species (ROS) are implicated in hepatic fibrosis development.
  • Ursolic acid (UA) demonstrated antifibrotic effects in vitro by inhibiting NOX-mediated signaling in hepatic stellate cells (HSCs).

Purpose of the Study:

  • To investigate the in vivo efficacy of ursolic acid (UA) in alleviating carbon tetrachloride (CCl4)-induced liver fibrosis.
  • To elucidate the mechanisms underlying UA's antifibrotic effects, focusing on NOX/ROS pathways in hepatocytes (HCs), HSCs, and Kupffer cells (KCs).

Main Methods:

  • CCl4-induced liver fibrosis model in vivo.
  • Assessment of UA's effects on NOX and ROS expression in HCs, HSCs, and KCs.
  • Evaluation of KC phagocytic activity (indices α and K).
  • Analysis of UA's impact on HC proliferation, HSC apoptosis, and KC activation.

Main Results:

  • UA alleviated CCl4-induced liver fibrosis by decreasing NOX and ROS expression across HCs, HSCs, and KCs.
  • UA treatment promoted HC proliferation and induced apoptosis in HSCs.
  • KC activation was prevented by UA, while phagocytic function remained unaffected.
  • UA did not compromise the host defense function.

Conclusions:

  • Ursolic acid (UA) effectively reverses liver fibrosis in vivo.
  • UA exerts its antifibrotic effects by modulating NOX/ROS pathways, promoting hepatocyte health, and inducing apoptosis in fibrogenic cells.
  • UA represents a potential therapeutic agent for liver fibrosis without compromising immune function.
Keywords:
Kupffer cellshepatic stellate cellshepatocytesursolic acid

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