Chymase inhibition attenuates lipopolysaccharide/ d-galactosamine-induced acute liver failure in hamsters

Pharmacology. 2014;93(1-2):47-56. doi: 10.1159/000357684. Epub 2014 Jan 17.

Abstract

Background/aims: Chymase inhibition has been shown to attenuate matrix metalloproteinase (MMP)-9 and tumor necrosis factor (TNF)-α, both of which are associated with the pathogenesis of acute liver failure (ALF). This study investigated the effects of the chymase inhibitor TY-51469 on lipopolysaccharide (LPS)/D-galactosamine (GalN)-induced ALF in hamsters.

Methods: TY-51469 (10 or 30 mg/kg) or placebo was administered 1 h before the LPS (160 µg/kg)/GalN (400 mg/kg) injection.

Results: Hepatic chymase activity was significantly increased after the LPS/GalN injection, but the significant increase was dose-dependently and significantly attenuated by treatment with TY-51469. Significant increases in hepatic MMP-9 activity and TNF-α concentration were observed after the LPS/GalN injection, but these increases were also attenuated by treatment with TY-51469. Plasma aspartate aminotransferase and alanine aminotransferase activities were significantly increased after LPS/GalN injection in the placebo-treated group, but the increases were significantly attenuated in the TY-51469-treated group. The area of hepatic necrotic after LPS/GalN injection was significantly reduced by treatment with TY-51469. Treatment with TY-51469 resulted in significant reductions in the hepatic malondialdehyde concentration, mast cell numbers, and gene expressions of interleukin-1β and myeloperoxidase.

Discussion: Chymase inhibition could be a useful strategy to attenuate LPS/GalN-induced ALF in hamsters.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Aspartate Aminotransferases / blood
  • Chymases / antagonists & inhibitors*
  • Chymases / metabolism
  • Galactosamine
  • Gene Expression
  • Interleukin-1beta / genetics
  • Lipopolysaccharides
  • Liver / drug effects
  • Liver / metabolism
  • Liver / pathology
  • Liver Failure, Acute / chemically induced
  • Liver Failure, Acute / drug therapy*
  • Liver Failure, Acute / metabolism
  • Liver Failure, Acute / pathology
  • Male
  • Malondialdehyde / metabolism
  • Matrix Metalloproteinase 9 / metabolism
  • Mesocricetus
  • Peroxidase / genetics
  • Sulfonamides / pharmacology
  • Sulfonamides / therapeutic use*
  • Thiophenes / pharmacology
  • Thiophenes / therapeutic use*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-1beta
  • Lipopolysaccharides
  • Sulfonamides
  • TY 51469
  • Thiophenes
  • Tumor Necrosis Factor-alpha
  • Malondialdehyde
  • Galactosamine
  • Peroxidase
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Chymases
  • Matrix Metalloproteinase 9