Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Dictamnus dasycarpus Turcz. alleviates cholestatic liver injury: orchestrating tissue-divergent extracellular matrix remodeling across the gut-liver axis.
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Li Yanan, Lv Chongning, Bai He, Li Jinghong, Leng Aijing, Chen Xiaoxia, Zhang Guixin, Qu Jialin
Аннотация
BACKGROUND: Cholestatic liver injury (CLI), characterized by disrupted bile flow resulting in hepatic inflammation and fibrosis, corresponds to "jaundice" in traditional Chinese medicine. Although Dictamnus dasycarpus Turcz. (Cortex Dictamni) has been historically documented for jaundice treatment, its efficacy and mechanisms remain unclear.
PURPOSE: This study investigates the hepatoprotective effects of Cortex Dictamni aqueous extract (CDAE) against CLI, focusing on its role in modulating the gut-liver axis to restore bile acid homeostasis and alleviate hepatic injury.
METHODS: An α-naphthylisothiocyanate (ANIT)-induced CLI mouse model was employed to evaluate the hepatoprotective effects of CDAE (0.65, 1.3, 2.6 g/kg, oral gavage). Comprehensive analyses included serum biochemistry, liver/ileum histopathological examination, bile acid metabolomics, 16S rDNA sequencing and transcriptomic profiling. Key phenotypic changes and candidate targets identified from screening were further confirmed using Western blot, RT-qPCR and Sirius Red staining.
RESULTS: CDAE significantly ameliorated CLI by dose-dependently reducing serum biomarkers (alanine aminotransferase; aspartate aminotransferase; total bilirubin; total bile acids), hepatosomatic index and hepatic necrosis. Mechanistically, it orchestrated bile acid homeostasis via activating the farnesoid X receptor/small heterodimer partner pathway, which downregulated hepatic cholesterol 7 alpha-hydroxylase (synthesis) and upregulated bile salt export pump and organic anion transporting polypeptide 1A1 (efflux). Moreover, CDAE counteracted ANIT-induced gut dysbiosis by enriching beneficial Lactobacillus and suppressing opportunistic Proteobacteria. Notably, CDAE exhibited tissue-divergent effects on extracellular matrix remodeling: it attenuated hepatic fibrogenesis by downregulating pro-fibrotic targets (collagen type I alpha 1, collagen type I alpha 2, elastin), while conversely promoting intestinal barrier repair by upregulating barrier-strengthening targets (collagen type I alpha 1, collagen type I alpha 2, thrombospondin-2, integrin alpha 8).
CONCLUSION: CDAE ameliorates CLI by reshaping gut microbiota and bile acid composition to restore homeostasis and activate the farnesoid X receptor/small heterodimer partner pathway, thereby orchestrating coordinated extracellular matrix remodeling across organs. These findings provide pharmacological and mechanism evidence for Cortex Dictamni's traditional use in jaundice.
PURPOSE: This study investigates the hepatoprotective effects of Cortex Dictamni aqueous extract (CDAE) against CLI, focusing on its role in modulating the gut-liver axis to restore bile acid homeostasis and alleviate hepatic injury.
METHODS: An α-naphthylisothiocyanate (ANIT)-induced CLI mouse model was employed to evaluate the hepatoprotective effects of CDAE (0.65, 1.3, 2.6 g/kg, oral gavage). Comprehensive analyses included serum biochemistry, liver/ileum histopathological examination, bile acid metabolomics, 16S rDNA sequencing and transcriptomic profiling. Key phenotypic changes and candidate targets identified from screening were further confirmed using Western blot, RT-qPCR and Sirius Red staining.
RESULTS: CDAE significantly ameliorated CLI by dose-dependently reducing serum biomarkers (alanine aminotransferase; aspartate aminotransferase; total bilirubin; total bile acids), hepatosomatic index and hepatic necrosis. Mechanistically, it orchestrated bile acid homeostasis via activating the farnesoid X receptor/small heterodimer partner pathway, which downregulated hepatic cholesterol 7 alpha-hydroxylase (synthesis) and upregulated bile salt export pump and organic anion transporting polypeptide 1A1 (efflux). Moreover, CDAE counteracted ANIT-induced gut dysbiosis by enriching beneficial Lactobacillus and suppressing opportunistic Proteobacteria. Notably, CDAE exhibited tissue-divergent effects on extracellular matrix remodeling: it attenuated hepatic fibrogenesis by downregulating pro-fibrotic targets (collagen type I alpha 1, collagen type I alpha 2, elastin), while conversely promoting intestinal barrier repair by upregulating barrier-strengthening targets (collagen type I alpha 1, collagen type I alpha 2, thrombospondin-2, integrin alpha 8).
CONCLUSION: CDAE ameliorates CLI by reshaping gut microbiota and bile acid composition to restore homeostasis and activate the farnesoid X receptor/small heterodimer partner pathway, thereby orchestrating coordinated extracellular matrix remodeling across organs. These findings provide pharmacological and mechanism evidence for Cortex Dictamni's traditional use in jaundice.