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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2005, Vol. 10 ›› Issue (2): 196-200.

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Effects of novel recombinant human tumor necrosis factor α(nrhTNFα) on liver injury induced by carbon tetrachloride or Concanavalin A

SHI Chuan-qun, WU Yong-jie, GAO Ming-tang, LI Wen-guang, ZANG Kai-hong, LI Zhi-qin   

  1. College of Pharmaceutical Science of Lanzhou University, Key Laboratory of Preclinical Study for New Traditional Chinese Medicine of Gansu Province Lanzhou, 730000, Gansu, China
  • Received:2004-11-01 Revised:2004-12-06 Online:2005-02-06 Published:2020-11-18

Abstract: AIM: To investigate the effects of different doses of nrhTNFαon liver function and liver histological morphology and explore its mechanism.METHODS: Liver injury was induced by CCl4 or Concanavalin A (Con A)in mice.nrhTNFα(IU°kg-1)was injected intramuscularly at low(5×104), median(5×105), and high doses (5×106).Changes of serum ALT, AST, LDH, IFN-γ, IL-2 and NO levels were detected.Liver histological changes were examined accordingly.RESULTS: The nrhTNFαhad no effect on the liver function and liver histological morphology in intact mice at above three doses groups.The nrhTNFαalso had no effect on the liver function and liver histological morphology in the CCl4-treated mice at the low and median doses groups, but liver damage was exacerbated at the high dose group in this model. The increased concentrations of serum ALT, AST, LDH and IFN-γlevels in the Con A-treated mice were diminished with three doses groups, especially at the low dose group.A significant improvement was observed in pathohistology examination in this model at above three doses groups.CONCLUSION: The nrhTNFαim has no hepatic toxicity in intact mice at above three doses groups.The low and median doses of nrhTNFαim have no impact on the liver injury in the CCl4-treatedmice.The high dose of nrhTNFαim exacerbates the liver injury in this model. The nrhTNFαinhibits the liver injury in the Con A-treated mice.Its mechanisms may be related to the inhibition of the production of IFN-γin this model.

Key words: tumorne crosis factor-α, liver injury, Concanavalin A(ConA), carbon tetrachloride, interferon-γ, mice

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