Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Tetrastigma hemsleyanum Diels & Gilg ameliorates alcohol-associated liver disease by modulating the gut-liver axis and ferroptosis.
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Zhan Lianghui, Liu Qian, Jiang Xuechun, Hu Yijuan, Zhou Jie, Zhu Sheng, Liang Weiqing, Pu Jinbao
Аннотация
BACKGROUND: Alcohol-associated liver disease (ALD) encompasses a spectrum of hepatic injuries driven by chronic inflammation and oxidative stress. Tetrastigma hemsleyanum Diels & Gilg rootlets principle (THRP) displays hepatoprotective potential. However, its systematic mechanisms along the gut-liver axis are not yet fully elucidated.
PURPOSE: To investigate the protective effects of THRP on ALD and elucidate its systemic regulation of microbial metabolites and hepatocyte fate.
METHODS: Mice were pretreated with THRP for 7 days, followed by a 7-day co-administration of THRP and 40% ethanol. Liver injury, intestinal barrier integrity, and iron homeostasis were evaluated. The underlying mechanisms were explored using 16S rRNA and scRNA-seq.
RESULTS: THRP partially alleviated alcohol-induced hepatic steatosis, inflammatory cell infiltration, and elevated liver enzyme levels. In the gut, THRP restored mucosal barrier integrity and suppressed the expansion of the pathobiont s_Cryptobacteroides, which was associated with increased polyamine biosynthesis and reduced systemic lipopolysaccharide translocation. Further, scRNA-seq and pseudotime analyses suggested that ferroptosis-related pathways were altered in alcohol-stressed hepatocytes and associated with THRP intervention. THRP treatment was associated with a favorable shift in this ferroptotic trajectory, concomitant with the upregulation of the NRf2-GPX4 axis and potential modulation of the fibroblast-to-hepatocyte bone morphogenetic protein (BMP) signaling crosstalk. THRP treatment was also associated with altered fibroblast-to-hepatocyte BMP signaling patterns and reduced hepatic iron accumulation.
CONCLUSIONS: THRP protects against ALD by regulating gut-liver axis homeostasis and inhibiting hepatic ferroptosis, including suppression of pathobionts. These findings support THRP as a natural candidate for further preclinical and clinical studies on ALD.
PURPOSE: To investigate the protective effects of THRP on ALD and elucidate its systemic regulation of microbial metabolites and hepatocyte fate.
METHODS: Mice were pretreated with THRP for 7 days, followed by a 7-day co-administration of THRP and 40% ethanol. Liver injury, intestinal barrier integrity, and iron homeostasis were evaluated. The underlying mechanisms were explored using 16S rRNA and scRNA-seq.
RESULTS: THRP partially alleviated alcohol-induced hepatic steatosis, inflammatory cell infiltration, and elevated liver enzyme levels. In the gut, THRP restored mucosal barrier integrity and suppressed the expansion of the pathobiont s_Cryptobacteroides, which was associated with increased polyamine biosynthesis and reduced systemic lipopolysaccharide translocation. Further, scRNA-seq and pseudotime analyses suggested that ferroptosis-related pathways were altered in alcohol-stressed hepatocytes and associated with THRP intervention. THRP treatment was associated with a favorable shift in this ferroptotic trajectory, concomitant with the upregulation of the NRf2-GPX4 axis and potential modulation of the fibroblast-to-hepatocyte bone morphogenetic protein (BMP) signaling crosstalk. THRP treatment was also associated with altered fibroblast-to-hepatocyte BMP signaling patterns and reduced hepatic iron accumulation.
CONCLUSIONS: THRP protects against ALD by regulating gut-liver axis homeostasis and inhibiting hepatic ferroptosis, including suppression of pathobionts. These findings support THRP as a natural candidate for further preclinical and clinical studies on ALD.