Antithrombin III prevents concanavalin A-induced liver injury through inhibition of macrophage inflammatory protein-2 release and production of prostacyclin in mice

J Hepatol. 2002 Jun;36(6):766-73. doi: 10.1016/s0168-8278(02)00059-4.

Abstract

Background/aims: Recently, we have reported that macrophage inflammatory protein-2 (MIP-2) plays a pivotal role in concanavalin A (Con A)-induced liver injury. In this study, we investigated the effect of antithrombin III (AT-III) on liver damage, and production of MIP-2 and prostacyclin in this model.

Methods: Liver injury was induced by intravenous injection of Con A (15 mg/kg) and AT-III was administered (50, 250 and 500 units/kg, iv) 30 mm before Con A injection. Plasma levels of alanine aminotransferase (ALT), MIP-2 and 6-keto-prostaglandin F1alpha (6k-PG-F1alpha), stable metabolite of prostaglandin I(2) (prostacyclin), were determined.

Results: The elevated plasma ALT levels 8, 16, 24 h after Con A injection were inhibited by AT-III pretreatment. The elevated plasma MIP-2 levels were significantly inhibited by AT-III pretreatment compared with vehicle treatment. The inhibitory effect of AT-III on plasma ALT and MIP-2 in Con A-induced liver injury was attenuated by indomethacin (5 mg/kg, ip). Plasma concentration of 6k-PG-F1alpha at 2 h after AT-III injection was significantly elevated compared with baseline and vehicle pretreatment.

Conclusions: These findings suggest that AT-III prevents Con A-induced liver injury through an inhibition of MIP-2 release and a production of prostacyclin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Antineoplastic Agents / pharmacology
  • Antithrombin III / pharmacology*
  • Chemical and Drug Induced Liver Injury
  • Chemokine CXCL2
  • Chemokines / metabolism*
  • Concanavalin A
  • Cytokines / biosynthesis
  • Epoprostenol / biosynthesis*
  • Epoprostenol / blood
  • Female
  • Indomethacin / pharmacology
  • Liver Diseases / drug therapy*
  • Liver Diseases / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Monokines / pharmacology
  • Neutrophils / immunology
  • Recombinant Proteins / pharmacology
  • Serine Proteinase Inhibitors / pharmacology*
  • Specific Pathogen-Free Organisms
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Antineoplastic Agents
  • Chemokine CXCL2
  • Chemokines
  • Cxcl2 protein, mouse
  • Cytokines
  • Monokines
  • Recombinant Proteins
  • Serine Proteinase Inhibitors
  • Tumor Necrosis Factor-alpha
  • Concanavalin A
  • Antithrombin III
  • Epoprostenol
  • Alanine Transaminase
  • Indomethacin