Journal of Practical Hepatology ›› 2025, Vol. 28 ›› Issue (6): 813-817.doi: 10.3969/j.issn.1672-5069.2025.06.004

• Hepatitis in mice • Previous Articles     Next Articles

Improvement of liver steatosis of Coprococcus eutactus in mice with MCD-induced metabolic-associated fatty liver disease

Yang Siqi, Chen Jiawei, Li Shaohan, et al   

  1. Department of Gastroenterology and Hepatology, Second Affiliated Hospital School of Medicine, South China University of Technology, Guangzhou 510180, Guangdong Province, China
  • Received:2025-04-27 Online:2025-11-10 Published:2025-11-13

Abstract: Objective This experiment aimed to observe improvement of liver steatosis of Coprococcus eutactus (C. eutactus) in mice with methionine-choline-deficent diet (MCD)-induced metabolic-associated fatty liver disease (MAFLD). Methods Two MAFLD mouse models, e.g., in db/db mice and in a MCD-induced mice, were established. The mice were randomly divided into control, model and C. eutactus –intervened (daily oral gavage of C. eutactus at 109 CFU/mouse) groups. After finishing the experiment, serum samples were collected for biochemical analysis, and liver tissues were subjected to Hematoxylin & Eosin staining, oil red O staining and Masson staining. Quantitative real-time PCR and Western blotting were applied to investigate gene and protein expression. Results Pathological examination showed marked improvements in hepatocyte steatosis and inflammatory infiltration; qPCR analysis demonstrated that C. eutactus intervention significantly down-regulated mRNA levels of lipid metabolism-related genes (such as FASN and Fabp5) in mouse liver tissues compared to in the model group (decreased by 44.1% and 52.7%, respectively, P<0.01); furthermore, C. eutactus intervention greatly suppressed protein expression of inflammatory cytokines, such as CCL3, and fibrosis markers, as TGF-β1, in hepatic tissues compared to either in the control or in the model groups. Conclusion This study confirms that C. eutactus could ameliorate liver steatosis by inhibiting lipid synthesis, reducing inflammatory responses, and delaying fibrosis progression.

Key words: Metabolic-associated fatty liver disease, Coprococcus eutactus, Lipid metabolism, Liver fibrosis, Mice