[Triptolide inhibits the inflammatory response of monocytes from rheumatoid arthritis patients by regulating miR-155]

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2014 Jun;30(6):635-8.
[Article in Chinese]

Abstract

Objective: To explore the anti-inflammatory effect of triptolide (TPT) by regulating miR-155 in monocytes pre-stimulated by lipopolysaccharide (LPS) from rheumatoid arthritis (RA) patients.

Methods: Monocytes were isolated by CD14⁺ magnetic beads from peripheral blood mononuclear cells (PBMCs) of RA and stimulated by LPS for 24 hours. The levels of tumor-necrosis factor-α (TNF-α) and interleukin 6 (IL-6) in monocytes were detected by ELISA and the expression of miR-155 was measured by real-time quantitative PCR (qRT-PCR) in monocytes before and after the treatment of TPT at different concentrations. MiR-155 mimic and negative control were respectively transfected into the LPS-stimulated monocytes by Lipofectamine(TM)2000. Twenty-four hours later, the monocytes were treated with or without TPT for another 24 hours. TNF-α and IL-6 expressions in the cell culture supernatants were detected by ELISA and the expressions of suppressor of cytokine signaling-1 (SOCS1) and Src homology 2 domain-containing inositol 5-phosphatase 1 (SHIP-1) were tested by Western blotting.

Results: TPT suppressed the expressions of TNF-α, IL-6 and miR-155 in LPS-stimulated peripheral blood monocytes from RA patients. Over-expression of miR-155 significantly reversed the down-regulation of TNF-α and IL-6 by TPT in monocytes. TPT up-regulated the expressions of SOCS1 and SHIP-1 in monocytes, but over-expressed miR-155 antagonized the effect of TPT on SHIP-1 while the expression of SOCS1 was not affected.

Conclusion: TPT suppressed the expression of miR-155 and up-regulated the release of SHIP-1, thus inhibiting the inflammatory response in the LPS-stimulated monocytes of RA patients.

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Arthritis, Rheumatoid / blood*
  • Arthritis, Rheumatoid / genetics
  • Arthritis, Rheumatoid / pathology
  • Blotting, Western
  • Cells, Cultured
  • Diterpenes / pharmacology*
  • Enzyme-Linked Immunosorbent Assay
  • Epoxy Compounds / pharmacology
  • Gene Expression Regulation / drug effects*
  • Humans
  • Inositol Polyphosphate 5-Phosphatases
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / pharmacology
  • MicroRNAs / genetics*
  • Monocytes / drug effects*
  • Monocytes / metabolism
  • Monocytes / pathology
  • Phenanthrenes / pharmacology*
  • Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases
  • Phosphoric Monoester Hydrolases / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Suppressor of Cytokine Signaling 1 Protein
  • Suppressor of Cytokine Signaling Proteins / metabolism
  • Tripterygium / chemistry
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Diterpenes
  • Epoxy Compounds
  • Interleukin-6
  • Lipopolysaccharides
  • MIRN155 microRNA, human
  • MicroRNAs
  • Phenanthrenes
  • SOCS1 protein, human
  • Suppressor of Cytokine Signaling 1 Protein
  • Suppressor of Cytokine Signaling Proteins
  • Tumor Necrosis Factor-alpha
  • triptolide
  • Phosphoric Monoester Hydrolases
  • Inositol Polyphosphate 5-Phosphatases
  • INPP5D protein, human
  • Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases