Inhibitory effects of armepavine against hepatic fibrosis in rats

J Biomed Sci. 2009 Sep 2;16(1):78. doi: 10.1186/1423-0127-16-78.

Abstract

Activation of hepatic stellate cells (HSCs) plays a crucial role in liver fibrogenesis. armepavine (Arm, C19H23O3N), an active compound from Nelumbo nucifera, has been shown to exert immunosuppressive effects on T lymphocytes and on lupus nephritic mice. The aim of this study was to investigate whether Arm could exert anti-hepatic fibrogenic effects in vitro and in vivo. A cell line of rat HSCs (HSC-T6) was stimulated with tumor necrosis factor-alpha (TNF-alpha) or lipopolysaccharide (LPS) to evaluate the inhibitory effects of Arm. An in vivo therapeutic study was conducted in bile duct-ligated (BDL) rats. BDL rats were given Arm (3 or 10 mg/kg) by gavage twice daily for 3 weeks starting from the onset of BDL. Liver sections were taken for fibrosis scoring, immuno-fluorescence staining and quantitative real-time mRNA measurements. In vitro, Arm (1-10 microM) concentration-dependently attenuated TNF-alpha- and LPS-stimulated alpha-SMA protein expression and AP-1 activation by HSC-T6 cells without adverse cytotoxicity. Arm also suppressed TNF-alpha-induced collagen collagen deposition, NFkappaB activation and MAPK (p38, ERK1/2, and JNK) phosphorylations. In vivo, Arm treatment significantly reduced plasma AST and ALT levels, hepatic alpha-SMA expression and collagen contents, and fibrosis scores of BDL rats as compared with vehicle treatment. Moreover, Arm attenuated the mRNA expression levels of col 1alpha2, TGF-beta1, TIMP-1, ICAM-1, iNOS, and IL-6 genes, but up-regulated metallothionein genes. Our study results showed that Arm exerted both in vitro and in vivo antifibrotic effects in rats, possibly through anti-NF-kappaB activation pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / biosynthesis
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
  • Anti-Inflammatory Agents, Non-Steroidal / toxicity
  • Benzylisoquinolines / pharmacology
  • Benzylisoquinolines / therapeutic use*
  • Benzylisoquinolines / toxicity
  • Cell Line / drug effects
  • Cell Line / ultrastructure
  • Collagen / biosynthesis
  • Drug Evaluation, Preclinical
  • Gene Expression Regulation / drug effects
  • Hepatic Stellate Cells / drug effects*
  • Hepatic Stellate Cells / ultrastructure
  • Immunosuppressive Agents / pharmacology
  • Immunosuppressive Agents / therapeutic use*
  • Immunosuppressive Agents / toxicity
  • Lipopolysaccharides / pharmacology
  • Liver Cirrhosis, Biliary / blood
  • Liver Cirrhosis, Biliary / drug therapy*
  • Liver Cirrhosis, Biliary / genetics
  • Liver Cirrhosis, Biliary / pathology
  • Liver Cirrhosis, Experimental / blood
  • Liver Cirrhosis, Experimental / drug therapy*
  • Liver Cirrhosis, Experimental / genetics
  • Liver Cirrhosis, Experimental / pathology
  • MAP Kinase Signaling System / drug effects
  • Male
  • NF-kappa B / metabolism
  • Nelumbo / chemistry
  • Phosphorylation
  • Phytotherapy*
  • Protein Processing, Post-Translational / drug effects
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Rats
  • Rats, Sprague-Dawley
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Actins
  • Anti-Inflammatory Agents, Non-Steroidal
  • Benzylisoquinolines
  • Immunosuppressive Agents
  • Lipopolysaccharides
  • NF-kappa B
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Collagen
  • armepavine