Salvianolic acid B and sodium tanshinone II A sulfonate prevent pulmonary fibrosis through anti-inflammatory and anti-fibrotic process

Eur J Pharmacol. 2020 Sep 15:883:173352. doi: 10.1016/j.ejphar.2020.173352. Epub 2020 Jul 6.

Abstract

Pulmonary fibrosis (PF) is an interstitial lung disease characterized by interstitial inflammation and fibrosis. Salvianolic acid B (SAB) and sodium tanshinone IIA sulfonate (STS) are representative components in Salvia miltiorrhiza, which have been reported using in the treatment of PF. The aim of the study was to explain the role of inflammation in the process of PF and to investigate the effect of SAB and STS on inflammation and fibrosis in vitro. The results clearly indicated that lipopolysaccharide (LPS)-stimulated inflammatory response could induce fibroblast proliferation and fibroblast to myofibroblast transformation (FMT). Both SAB and STS significantly inhibited LPS-induced inflammation in vitro, including down-regulated the protein expression levels of IL-1β and TNF-α and the mRNA expression levels of IL1B and TNFA. Furthermore, both SAB and STS inhibited TGF-β1-induced the proliferation in MRC-5 cells and the overexpression of α-SMA and COL1α1, both the protein and mRNA levels. In conclusion, these results indicate that the inflammatory response is necessary for the development of PF, and the therapeutic effect of SAB and STS on PF may be related to anti-inflammatory and anti-fibrotic effects.

Keywords: Inflammation; Pulmonary fibrosis; Salvianolic acid B; Sodium tanshinone IIA sulfonate; TGF-β1.

MeSH terms

  • Actins / genetics
  • Actins / metabolism
  • Anti-Inflammatory Agents / pharmacology*
  • Benzofurans / pharmacology*
  • Cell Proliferation / drug effects
  • Coculture Techniques
  • Collagen Type I / genetics
  • Collagen Type I / metabolism
  • Collagen Type I, alpha 1 Chain
  • Cytokines / genetics
  • Cytokines / metabolism
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Humans
  • Inflammation Mediators / metabolism
  • Lung / drug effects*
  • Lung / metabolism
  • Lung / pathology
  • Macrophages / drug effects*
  • Macrophages / metabolism
  • Macrophages / pathology
  • Phenanthrenes / pharmacology*
  • Pneumonia / metabolism
  • Pneumonia / pathology
  • Pneumonia / prevention & control*
  • Pulmonary Fibrosis / metabolism
  • Pulmonary Fibrosis / pathology
  • Pulmonary Fibrosis / prevention & control*
  • THP-1 Cells

Substances

  • ACTA2 protein, human
  • Actins
  • Anti-Inflammatory Agents
  • Benzofurans
  • Collagen Type I
  • Collagen Type I, alpha 1 Chain
  • Cytokines
  • Inflammation Mediators
  • Phenanthrenes
  • tanshinone II A sodium sulfonate
  • salvianolic acid B