Journal of ethnopharmacology · 2025
Yinchenzhufu decoction ameliorates cholestatic liver injury through decreasing the formation of neutrophil extracellular traps in mice.
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Li Qi, Meng Qian, Niu Ningning, Li Yiqian, Lu Wenye, Wang Tianming, Li Yuanyuan, Ju Wanjun, Ma Yueming, Wu Jiasheng
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Neutrophil extracellular traps (NETs) are important driving factors to liver disease. Yinchenzhufu decoction (YCZFD) is a classical traditional herbal medicine used to treat cholestatic liver injury (CLI); however, its effect on NETs in CLI remains unknown.
AIM OF THE STUDY: To elucidate the potential molecular mechanism of YCZFD against CLI through multiple omics techniques.
MATERIALS AND METHODS: The protective effects of YCZFD against cholestatic liver injury and fibrosis were investigated in a 3, 5-Diethoxycarbonyl-1, 4-Dihydro-2, 4, 6-Collidine (DDC) induced cholestatic mouse model. Its effects on blood biochemical indicators, liver tissue morphology, neutrophil infiltration, and fibrosis in cholestatic mice were determined. Then RNA sequencing, quantitative proteomics, and molecular biology were used to analyze the mechanism of YCZFD against CLI.
RESULTS: Treatment different doses of YCZFD significantly ameliorated neutrophil infiltration, alleviating CLI in cholestatic mice. RNA sequencing showed that neutrophil recruitment genes, such as CXCL5 and CXCR2, were upregulated in the liver tissues of cholestatic mice, but YCZFD treatment decreased this expression. Additionally, quantitative proteomics revealed that liver myeloperoxidase and S100A9 expression, key marker proteins of NETs, was significantly increased in cholestatic mice and decreased by YCZFD. Similarly, molecular biology confirmed that YCZFD reduced NETs proteins expression and ameliorated NETs formation in the liver of cholestatic mice. As NETs promotes inflammation, further results showed that YCZFD treatment inhibited the NF-κB signaling pathway and collagen formation, alleviating liver inflammation and fibrosis of cholestatic mice.
CONCLUSIONS: YCZFD decreases neutrophil recruitment and formation of NETs, in turn alleviating cholestatic liver injury and fibrosis.
AIM OF THE STUDY: To elucidate the potential molecular mechanism of YCZFD against CLI through multiple omics techniques.
MATERIALS AND METHODS: The protective effects of YCZFD against cholestatic liver injury and fibrosis were investigated in a 3, 5-Diethoxycarbonyl-1, 4-Dihydro-2, 4, 6-Collidine (DDC) induced cholestatic mouse model. Its effects on blood biochemical indicators, liver tissue morphology, neutrophil infiltration, and fibrosis in cholestatic mice were determined. Then RNA sequencing, quantitative proteomics, and molecular biology were used to analyze the mechanism of YCZFD against CLI.
RESULTS: Treatment different doses of YCZFD significantly ameliorated neutrophil infiltration, alleviating CLI in cholestatic mice. RNA sequencing showed that neutrophil recruitment genes, such as CXCL5 and CXCR2, were upregulated in the liver tissues of cholestatic mice, but YCZFD treatment decreased this expression. Additionally, quantitative proteomics revealed that liver myeloperoxidase and S100A9 expression, key marker proteins of NETs, was significantly increased in cholestatic mice and decreased by YCZFD. Similarly, molecular biology confirmed that YCZFD reduced NETs proteins expression and ameliorated NETs formation in the liver of cholestatic mice. As NETs promotes inflammation, further results showed that YCZFD treatment inhibited the NF-κB signaling pathway and collagen formation, alleviating liver inflammation and fibrosis of cholestatic mice.
CONCLUSIONS: YCZFD decreases neutrophil recruitment and formation of NETs, in turn alleviating cholestatic liver injury and fibrosis.