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OA

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.