Pepstatin A attenuates the inhibitory effect of N-acetyl-L-cysteine on proliferation of hepatic myofibroblasts (stellate cells)

Eur J Pharmacol. 2002 Sep 20;451(3):265-70. doi: 10.1016/s0014-2999(02)02296-3.

Abstract

The pharmacological interaction between pepstatin A, a specific inhibitor of cathepsin D, and N-acetyl-L-cysteine was analyzed using hepatic stellate cells in primary culture. Isolated rat stellate cells were cultured on plastic dishes in Dulbecco's modified Eagle's medium (DMEM). Proteins and phospho-proteins were detected by Western blot. DNA synthesis was determined by [3H]thymidine uptake. Pepstatin A restored DNA synthesis of stellate cells stimulated by either platelet-derived growth factor-BB (PDGF-BB) or insulin-like growth factor-I (IGF-I), an effect that was attenuated by N-acetyl-L-cysteine. This agent induced the recovery of both the expression of PDGF receptor beta and IGF-I receptor beta and the phosphorylation of p42/44 mitogen-activated protein kinase (MAPK) and Akt under stimulation with either PDGF-BB or IGF-I, which were downregulated by N-acetyl-L-cysteine. Expression of cathepsin D was induced in activated stellate cells. These results indicate that pepstatin A hampers the inhibitory effect of N-acetyl-L-cysteine on stellate cell growth by ameliorating growth factor receptor downregulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcysteine / antagonists & inhibitors*
  • Acetylcysteine / pharmacology
  • Animals
  • Cathepsin D / antagonists & inhibitors*
  • Cells, Cultured
  • Down-Regulation
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • Pepstatins / pharmacology*
  • Rats
  • Rats, Wistar
  • Signal Transduction / drug effects
  • Thymidine / metabolism

Substances

  • Pepstatins
  • Cathepsin D
  • pepstatin
  • Thymidine
  • Acetylcysteine