Atractylenolide I prevents acute liver failure in mouse by regulating M1 macrophage polarization

Atractylenolide I prevents acute liver failure in mouse by regulating M1 macrophage polarization

Abstract Acute liver failure (ALF) is a life-threatening clinical syndrome with a substantial risk of mortality. A murine model of lipopolysaccharide (LPS)- and D-galactosamine (D-GalN)-induced ALF is widely used to investigate the underlying mechanisms and potential therapeutic drugs for human live...

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Main Authors: Hui Zhang, Min Gao, Haiyan Wang, Junfeng Zhang, Lin Wang, Guanjun Dong, Qun Ma, Chunxia Li, Jun Dai, Zhihua Li, Fenglian Yan, Huabao Xiong
Format: Article
Language:English
Published: Nature Portfolio 2025-02-01
Series:Scientific Reports
Subjects:
Acute liver failure
Atractylenolide I
M1 macrophage polarization
Inflammation
Oxidative stress
Online Access:https://doi.org/10.1038/s41598-025-86977-x
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Summary:Abstract Acute liver failure (ALF) is a life-threatening clinical syndrome with a substantial risk of mortality. A murine model of lipopolysaccharide (LPS)- and D-galactosamine (D-GalN)-induced ALF is widely used to investigate the underlying mechanisms and potential therapeutic drugs for human liver failure. Atractylenolide I (ATR-I) is an active component of the Atractylodes macrocephala rhizome and possesses various pharmacological activities, including anti-tumor, anti-inflammatory, and anti-oxidant properties. Given the key role of oxidative stress and inflammation in ALF pathogenesis, this study investigates the protective effects of ATR-I on LPS/D-GalN-induced ALF in mice. The results suggest that ATR-I pretreatment significantly ameliorates ALF, as evidenced by decreased serum aminotransferase levels and prolonged mice survival. Additionally, ATR-I pretreatment inhibits oxidative stress. Furthermore, the ATR-I pretreatment markedly suppresses M1 macrophage activation in hepatic mononuclear cells. In vitro experiments with bone marrow-derived macrophages indicate that ATR-I regulates macrophage polarization through the mitogen-activated protein kinase (MAPK) and interferon regulatory factor (IRF) signaling pathways. Collectively, ATR-I pretreatment protects mice from LPS/D-GalN-induced ALF partially by regulating M1 macrophage polarization.
ISSN:2045-2322

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