实用肝脏病杂志 ›› 2026, Vol. 29 ›› Issue (1): 13-16.doi: 10.3969/j.issn.1672-5069.2026.01.004

• 实验性肝炎 • 上一篇    下一篇

甜菜碱通过调节JNK/STAT3信号通路缓解LPS/D-gal诱导的急性肝衰竭小鼠肝损伤实验研究*

罗轲, 王钰鲲, 郭金, 石春霞, 龚作炯   

  1. 430060 武汉市 武汉大学人民医院感染病科
  • 收稿日期:2025-07-02 出版日期:2026-01-10 发布日期:2026-02-04
  • 通讯作者: 龚作炯,E-mail: zjgong@163.com
  • 作者简介:罗轲,男,24岁,硕士研究生。主要从事急慢性肝病防治研究。E-mail: lk15623008277@163.com
  • 基金资助:
    *国家自然科学基金资助项目(编号:82270627)

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

摘要: 目的 探讨甜菜碱保护急性肝衰竭(ALF)小鼠肝损伤的作用机制。方法 将30只C57BL/6J小鼠随机分为对照组、模型组、小剂量、中剂量和大剂量甜菜碱处理组,采用LPS/D-gal腹腔注射建立ALF模型,采用Western blot法检测小鼠肝组织信号转导和转录激活因子3(STAT3)、p-STAT3、c-Jun N端激酶(JNK)和p-JNK表达水平。结果 LPS/ D-gal诱导小鼠ALF成功,甜菜碱处理改善了肝组织学损伤;模型组小鼠血清ALT和AST水平分别为(1924.9±100.0)U/L和(2363.3±80.3)U/L,较对照组显著升高(P<0.05),而中剂量甜菜碱处理组小鼠血清ALT和AST水平分别为 【(369.1±37.9)U/L和(408.4±41.6)U/L】,较模型组显著降低(P<0.05);甜菜碱处理显著上调了STAT3(Tyr705)磷酸化,并下调了JNK(Thr183/Tyr185)磷酸化水平(P<0.05)。结论 甜菜碱通过抑制JNK活化并激活STAT3缓解ALF小鼠肝损伤,发挥了护肝作用。

关键词: 急性肝衰竭, 甜菜碱, c-Jun N端激酶, 信号转导和转录激活因子3, 小鼠

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