International immunopharmacology · 2026
Emodin inhibits the formation of gallstones by affecting the intestinal flora and expression of hepatic HIF1α.
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Liu Tianming, Wang Heming, Lu Dongxu, Yan Cong, Hang Fenghe, Ma Biao, Meng Xianzhi
Аннотация
BACKGROUND: Gallstone disease is a prevalent digestive disorder worldwide; however, current therapeutic approaches remain limited. Emodin, a natural anthraquinone compound, exerts diverse biological effects including anti-inflammatory activity and metabolic regulation. To elucidate the mechanism by which emodin inhibits gallstone formation, we conducted in vivo experiments, multi-omics analysis, and network pharmacology.
METHODS: Six-week-old C57BL/6 mice were used to establish an in vivo model with emodin intervention. Fecal microbiota transplantation (FMT), 16S rRNA gene sequencing, and serum metabolomics sequencing were employed to investigate the effects of emodin on gut microbiota and serum metabolites. Network pharmacology was applied to predict the regulatory effects of emodin on liver-related genes, which were further verified by fundamental experiments. The correlations between gut microbiota, serum metabolites, and liver genes were explored. Statistical analysis was performed using GraphPad Prism 9.0.
RESULTS: The medium dose of emodin (30 mg/kg) showed the optimal inhibitory effect on gallstones formation. Emodin reshaped the intestinal flora structure in mice with gallstones and increased the abundance of Limosilactobacillus reuteri (L. reuteri) in vivo. By elevating serum tauroursodeoxycholic acid (TUDCA) levels in mice, emodin downregulated the expression of hepatic HIF1α and upregulated the expression of AQP8.
CONCLUSIONS: Emodin inhibited gallstone formation in mice through two complementary mechanisms. First, emodin modulated the gut microbiota to promote the proliferation of L. reuteri; second, it increased serum TUDCA levels, thereby regulating the HIF1α-AQP8 pathway to alleviate cholestasis. In addition, we speculate that L. reuteri may elevate serum TUDCA content via several indirect pathways.
METHODS: Six-week-old C57BL/6 mice were used to establish an in vivo model with emodin intervention. Fecal microbiota transplantation (FMT), 16S rRNA gene sequencing, and serum metabolomics sequencing were employed to investigate the effects of emodin on gut microbiota and serum metabolites. Network pharmacology was applied to predict the regulatory effects of emodin on liver-related genes, which were further verified by fundamental experiments. The correlations between gut microbiota, serum metabolites, and liver genes were explored. Statistical analysis was performed using GraphPad Prism 9.0.
RESULTS: The medium dose of emodin (30 mg/kg) showed the optimal inhibitory effect on gallstones formation. Emodin reshaped the intestinal flora structure in mice with gallstones and increased the abundance of Limosilactobacillus reuteri (L. reuteri) in vivo. By elevating serum tauroursodeoxycholic acid (TUDCA) levels in mice, emodin downregulated the expression of hepatic HIF1α and upregulated the expression of AQP8.
CONCLUSIONS: Emodin inhibited gallstone formation in mice through two complementary mechanisms. First, emodin modulated the gut microbiota to promote the proliferation of L. reuteri; second, it increased serum TUDCA levels, thereby regulating the HIF1α-AQP8 pathway to alleviate cholestasis. In addition, we speculate that L. reuteri may elevate serum TUDCA content via several indirect pathways.