4.1 Article

The inhibitory effect of salvianolic acid B on TGF-β1-induced proliferation and differentiation in lung fibroblasts

Journal

EXPERIMENTAL LUNG RESEARCH
Volume 40, Issue 4, Pages 172-185

Publisher

TAYLOR & FRANCIS INC
DOI: 10.3109/01902148.2014.895070

Keywords

differentiation; fibroblasts; pulmonary fibrosis; salvianolic acid B; transforming growth factor-beta 1

Funding

  1. National Natural Science Foundation of China (NSFC) [81100042]
  2. Guangdong Medical Science Research Foundation [A2012498]
  3. Guangzhou Medical and Health Science Research Foundation [20121A011044]

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Salvianolic acid B (Sal B), one of the major water-soluble compounds of Danshen (a popular Chinese herb), possesses many of the biological activities, such as antifibrogenic effect in liver and renal diseases. Transforming growth factor-beta 1 (TGF-beta 1) plays a central role in the development of pulmonary fibrosis by stimulating extracellular matrix (ECM) accumulation and activating fibroblasts. Here, we investigated the effects of Sal B on cell proliferation, collagen synthesis, endogenous TGF-beta 1 production, and alpha-smooth muscle actin (alpha-SMA, a marker of myofibroblasts) expression in human lung fibroblasts stimulated by TGF-beta 1 in vitro. The cell proliferation rates were analyzed by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide) assay. The expression of TGF-beta 1 and type I collagen at both the mRNA and protein levels was detected by reverse transcription polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and radioimmunoassay, respectively. The a-SMA expression was detected by Western blot. TGF-beta 1 treatment of lung fibroblasts increased cell proliferation rates, and enhanced the expression level of type I collagen, endogenous TGF-beta 1 production, and a-SMA expression (P < .05). The treatment with only Sal B did not affect the proliferation and differentiation of lung fibroblasts. Interestingly, Sal B was found to inhibit TGF-beta 1-induced cell proliferation, expression of type I collagen, endogenous TGF-beta 1 production, and alpha-SMA expression in lung fibroblasts. Moreover, the inhibitory effect of Sal B on TGF-beta 1-induced proliferation and differentiation in lung fibroblasts was more significant when treated with high-dose Sal B (1 mu mol/L versus 10 mu mol/L, P < .05). These data demonstrate that Sal B inhibits TGF-beta 1-induced cell proliferation and differentiation in vitro experiment.

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