Format

Send to:

Choose Destination
See comment in PubMed Commons below
Eur J Pharmacol. 2013 Apr 15;706(1-3):36-40. doi: 10.1016/j.ejphar.2013.02.051. Epub 2013 Mar 16.

Taurochenodeoxycholic acid induces apoptosis of fibroblast-like synoviocytes.

Author information

  • 1Key Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture, College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, China.

Abstract

Recent evidences have suggested that the paucity of the apoptosis of fibroblast-like synoviocytes (FLS) may contribute to the pathogenesis of rheumatoid arthritis. Apoptosis induction of rheumatoid arthritis FLS is therefore suggested as a potential therapeutic approach for rheumatoid arthritis. Taurochenodeoxycholic acid (TCDCA), one of the main bioactive substances of animals' bile acid, could favorably ameliorate the progression development and bone destruction of adjuvant arthritis in rat. In this study, we aimed to investigate the possible effect of TCDCA on apoptosis induction of adjuvant arthritis FLS and the mechanisms involved in this process. Apoptosis was determined by flow cytometric analysis. Gene expression levels and the activities of caspase-3 and caspase-8 were evaluated using real time RT-PCR and luminogenic substrates. The activity of nuclear factor-κB (NF-κB) was measured by ELISA. The results showed TCDCA significantly enhanced the apoptosis of adjuvant arthritis FLS in a dose-dependent manner. Besides, TCDCA treatment markedly increased the gene expression level and activity of both caspase-3 and caspase-8. It could suppress the DNA-biding activity of NF-κB. We concluded TCDCA represented an apoptotic effect on adjuvant arthritis FLS via the activation of caspase cascade and this process may be mediated by NF-κB signaling pathway. It was suggested that TCDCA may be a potential therapeutic agent for rheumatoid arthritis.

Copyright © 2013 Elsevier B.V. All rights reserved.

PMID:
23510744
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk