[Effect of glycyrrhetinic acid on the expression of inflammatory factors in fibroblast-like synovial cells from collagen induced arthritis rats]

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2012 Sep;28(9):915-9.
[Article in Chinese]

Abstract

Aim: To determine the effects of glycyrrhetinic acid (GA), methotrexate(MTX) and GA+MTX on the expressions of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in fibroblast-like synovial (FLS) cells from collagen induced arthritis (CIA) rats.

Methods: CIA-FLS cells were isolated and purified from the synovium of CIA rats by tissue block culture method, and then treated with MTX, GA, GA+MTX or nothing (control group), respectively. Each group was cultured for 3 different time periods (1, 3, 5 d). Real-time qPCR was used to detect the expressions of TNF-α and IL-1β mRNA in CIA-FLS cells and ELISA to determine the levels of TNF-α and IL-1β in the supernatant.

Results: Day 1: No significant down-regulation of TNF-α and IL-1β mRNA was identified in intervention groups compared with the control group (P>0.05); Day 3: Intervention groups significantly down-regulated TNF-α and IL-1β mRNA (P<0.05 vs control), but without intergroup difference(P>0.05); Day 5: the three intervention groups all suppressed the expressions of TNF-α and IL-1β mRNA(P<0.05 vs control), with GA+MTX>MTX>GA in inhibiting effect (P<0.05). All intervention groups were found to inhibit the expressions of TNF-α and IL-1β in a time-dependent manner (P<0.05). Similar outcomes were observed in the change of the levels of TNF-α and IL-1β in cell culture supernatant by ELISA.

Conclusion: GA, MTX, GA+MTX suppress the expression of TNF-α and IL-1β in CIA-FLS cells in a time-dependent manner, and the suppressing effect is GA+MTX>MTX>GA.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arthritis, Experimental / drug therapy*
  • Arthritis, Experimental / metabolism
  • Cell Separation
  • Cells, Cultured
  • Fibroblasts / metabolism
  • Glycyrrhetinic Acid / pharmacology*
  • Interleukin-1beta / analysis*
  • Interleukin-1beta / genetics
  • Male
  • Methotrexate / pharmacology
  • RNA, Messenger / analysis
  • Rats
  • Rats, Sprague-Dawley
  • Synovial Fluid / cytology
  • Synovial Fluid / metabolism*
  • Tumor Necrosis Factor-alpha / analysis*
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Interleukin-1beta
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Glycyrrhetinic Acid
  • Methotrexate