A murine model of LPS/D-gal-induced acute hepatitis and alterations in mTOR signaling
Received:January 04, 2005  
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DOI:10.3969/j.issn.1005-4847.2015.03.016
KeyWord:LPS/D-gal;Acute hepatitis;Apoptosis;Murine model
                       
AuthorInstitution
李晓菲 中国医学科学院和北京协和医学院医学生物学研究所感染与免疫学实验室, 昆明
陶玉芬 中国医学科学院和北京协和医学院医学生物学研究所感染与免疫学实验室, 昆明
刘建生 中国医学科学院和北京协和医学院医学生物学研究所感染与免疫学实验室, 昆明
李超 中国医学科学院和北京协和医学院医学生物学研究所感染与免疫学实验室, 昆明
梁新新 中国医学科学院和北京协和医学院医学生物学研究所感染与免疫学实验室, 昆明
叶尤松 中国医学科学院医学生物学研究所小动物实验部, 昆明
唐东红 中国医学科学院医学生物学研究所小动物实验部, 昆明
刘红旗 中国医学科学院和北京协和医学院医学生物学研究所感染与免疫学实验室, 昆明
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Abstract:
      Objective To explore the changes of mTOR signaling in LPS/D-gal-induced acute hepatitis in mice. Methods Twenty-six healthy adult female ICR mice were divided into two groups: the control group and experimental group, 13 mice in each group. LPS/D-gal was used to induce acute hepatitis in the mice. The survival of mice was monitored within 24 hours after LPS/D-gal challenge. At 6 hours after challenge, samples of serum and liver tissue were collected for further analysis.Results Injection of LPS/D-gal resulted in acute death of the mice within 24 hours. At 6 hours post LPS/D-gal injection, the blood levels of ALT and AST were significantly increased. The mRNA expression of inflammatory cytokines Tnfa and Il6 was up-regulated in LPS/D-gal-induced hapatitis, in which DNA fragmentation and activation of caspase-3 were subsequently observed. Immunoblot analysis showed that both mTOR pathway and NF-κB pathway were activated. Unexpectedly, inhibition of mTOR signaling could neither decrease the apoptosis in the liver nor increase the survival of mice. Conclusions The results of the present study indicate that mTOR signaling may play pleiotropic roles in the pathogenesis of LPS/D-gal-induced hepatitis.
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