Journal of Practical Hepatology ›› 2026, Vol. 29 ›› Issue (1): 13-16.doi: 10.3969/j.issn.1672-5069.2026.01.004

• Hepatitis in mice • Previous Articles     Next Articles

Betaine alleviates LPS/D-gal-induced acute liver failure in mice by modulating JNK/STAT3 signaling pathway

Luo Ke, Wang Yukun, Guo Jin, et al   

  1. Department of Infectious Disease, Renmin Hospital Affiliated to Wuhan University, Wuhan 430060, Hubei Province, China
  • Received:2025-07-02 Online:2026-01-10 Published:2026-02-04

Abstract: Objective The aim of this study was to investigate the protective effect of betaine on liver injury in mice with LPS/D-gal-induced acute liver failure (ALF). Methods 30 C57BL/6J mice were randomly divided into control model, low-dose, medium-doseand high-dose of betaine-intervened groups, and the model of ALF was established by LPS/D-gal intraperitoneal injection. Western blotting was performed to detect hepatic expression of signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 (p-STAT3), c-Jun N-terminal kinase (JNK) and phosphorylated JNK (p-JNK). Results LPS/D-gal injection successfully induced liver failure model with significant liver tissue congestion, structural disruption and inflammatory cell infiltration, and the betaine intervention alleviated liver pathological damages; serum ALT and AST levels in the model group were (1924.9±100.0) U/L and (2363.3±80.3) U/L, both significantly higher than in the control group, while they decreased greatly in low-, medium- and high-doses of betaine-intervened groups (P<0.05); betaine intervention increased remarkably the phosphorylation of STAT3 (Tyr705) and decreased the phosphorylation of JNK (Thr183/Tyr185) expression (P<0.05). Conclusion Betaine ameliorates liver injury in mice with ALF, might by inhibiting JNK activation and promoting STAT3 activation.

Key words: Acute liver failure, Betaine, c-Jun N-terminal kinase, Signal transducer and activator of transcription 3, Mice