IL-32γ inhibits acetaminophen-induced acute hepatotoxicity through inactivation of NF-κB and STAT1 signals

Y. R. Kim, Y. S. Jung, Y. H. Lee, C. J. Hwang, J. L. Hwang, C. H. Seok, H. C. Seong, N. Y. Yoon, S. Y. Yeom, S. B. Han, D. Y. Yoon, Jin Tae Hong

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Abstract

Although several studies have shown physiological functions of interleukin (IL)-32, the role of IL-32 in liver has not yet been reported. This study was initiated to examine the effects of IL-32γ on APAP-induced acute hepatic failure in IL-32γ transgenic mice. IL-32γ overexpressing and non-transgenic mice received 500 mg/kg Acetoaminophen (APAP) intraperitoneally. Serum alanine transaminase and aspartate transaminase were significantly lower in the APAP treated IL-32γ overexpressing mice compared with those APAP-treated non-transgenic. IL-32γ markedly reduced a restricted area of the necrosis and inflammation. APAP-induced reduced glutathione depletion, induction of nitric oxide and lipid peroxidation, and cytochrome P4502E1 expression was significantly lowered in the IL-32γ overexpressing mice. Elevation of Kupffer cells and natural killer cells by APAP were reduced in the IL-32γ overexpressing mice. The expression of IL-1α, IL-1ra, macrophage inflammatory protein-2, C-C motif chemokine ligand 5 and tissue inhibitor of metalloproteinase-1 was increased by APAP in nontransgenic mice, and were lowered in the IL-32γ overexpressing mice. Moreover, APAP-induced nuclear transcription factor-kappa B (NF-κB) and signal transducers and activators of transcription 1 (STAT1) activities were greatly lowered in the IL-32γ overexpressing mice. The results indicate that IL-32γ could effectively inhibit drug-induced hepatic failure, and reduce the number of cytotoxic immune cells and pro-inflammatory cytokine production through reduced activities of NF-κB and STAT1. This might be attributable to lowering APAP-induced liver toxicity in IL-32γ overexpressing mice.

Original languageEnglish
Pages (from-to)663-674
Number of pages12
JournalEuropean Journal of Inflammation
Volume11
Issue number3
DOIs
Publication statusPublished - 2013

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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    Kim, Y. R., Jung, Y. S., Lee, Y. H., Hwang, C. J., Hwang, J. L., Seok, C. H., Seong, H. C., Yoon, N. Y., Yeom, S. Y., Han, S. B., Yoon, D. Y., & Hong, J. T. (2013). IL-32γ inhibits acetaminophen-induced acute hepatotoxicity through inactivation of NF-κB and STAT1 signals. European Journal of Inflammation, 11(3), 663-674. https://doi.org/10.1177/1721727X1301100310