5-HT2A receptor antagonists inhibit hepatic stellate cell activation and facilitate apoptosis

Liver Int. 2013 Apr;33(4):535-43. doi: 10.1111/liv.12110. Epub 2013 Jan 31.

Abstract

Background: 5-hydroxytryptamine (5-HT) receptors are upregulated in activated hepatic stellate cells (HSCs), and are therefore thought to play an important role in their activation.

Aim: The aim of this study was to determine whether 5-HT2A receptor antagonists affect the activation or apoptosis of HSCs in vitro and/or in vivo.

Methods: For the in vitro experiments, the viability, apoptosis and wound healing ability of LX-2 cells were examined after treatment with various 5-HT2A receptor antagonists. Levels of HSC activation markers (procollagen type I, α-SMA, TGF-β and Smad 2/3) were measured. For in vivo experiments, rats were divided into three groups: (i) a control group, (ii) a disease group, in which cirrhosis was induced by thioacetamide (iii) a treatment group, in which cirrhosis was induced and a 5-HT2A receptor antagonist (sarpogrelate, 30 mg/kg) was administered.

Results: 5-HT2A , but not 5-HT2B receptor mRNA increased with time upon HSC activation. 5-HT2A receptor antagonists (ketanserin and sarpogrelate) inhibited viability and wound healing in LX-2 cells and induced apoptosis. Expression of α-SMA and procollagen type I was also inhibited. In the in vivo study, lobular inflammation was reduced in the sarpogrelate-treated group, but there was only slight and statistically insignificant attenuation of periportal fibrosis. Expression of α-SMA, TGF-β and Smad 2/3 was also reduced in the treatment group.

Conclusions: 5-HT2A receptor antagonists can reduce inflammation and the activation of HSCs in this cirrhotic model.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Apoptosis / drug effects*
  • Cell Line
  • Cell Survival / drug effects
  • Collagen Type I / metabolism
  • Dose-Response Relationship, Drug
  • Hepatic Stellate Cells / drug effects*
  • Hepatic Stellate Cells / metabolism
  • Hepatic Stellate Cells / pathology
  • Humans
  • Ketanserin / pharmacology
  • Liver Cirrhosis, Experimental / chemically induced
  • Liver Cirrhosis, Experimental / drug therapy
  • Liver Cirrhosis, Experimental / metabolism
  • Liver Cirrhosis, Experimental / pathology
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species / metabolism
  • Receptor, Serotonin, 5-HT2A / drug effects*
  • Receptor, Serotonin, 5-HT2A / genetics
  • Receptor, Serotonin, 5-HT2A / metabolism
  • Ritanserin / pharmacology
  • Serotonin 5-HT2 Receptor Antagonists / pharmacology*
  • Smad2 Protein / metabolism
  • Smad3 Protein / metabolism
  • Succinates / pharmacology
  • Thioacetamide
  • Time Factors
  • Transforming Growth Factor beta / metabolism
  • Wound Healing / drug effects

Substances

  • ACTA2 protein, human
  • Actins
  • Collagen Type I
  • RNA, Messenger
  • Reactive Oxygen Species
  • Receptor, Serotonin, 5-HT2A
  • SMAD2 protein, human
  • SMAD3 protein, human
  • Serotonin 5-HT2 Receptor Antagonists
  • Smad2 Protein
  • Smad2 protein, rat
  • Smad3 Protein
  • Smad3 protein, rat
  • Succinates
  • Transforming Growth Factor beta
  • Thioacetamide
  • Ritanserin
  • sarpogrelate
  • Ketanserin