Protective role of gambogic acid in experimental pulmonary fibrosis in vitro and in vivo

Phytomedicine. 2016 Apr 15;23(4):350-8. doi: 10.1016/j.phymed.2016.01.011. Epub 2016 Feb 9.

Abstract

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive disorder with poor prognosis. The treatment options for IPF are very limited. Gambogic acid (GA) has anticancer effect and anti-proliferative activity which is extracted from a dried yellow resin of the Garcinia hanburyi Hook.f. [Clusiaceae (Guttiferae)] in Southeast Asia. However, the anti-fibrotic activities of GA have not been previously investigated.

Methods: In this study, the effects of GA on TGF-β1-mediated epithelial-mesenchymal transition (EMT) in A549 cells and endothelial-mesenchymal transition (EndoMT) in human pulmonary microvascular endothelial cells (HPMECs), on the proliferation of human lung fibroblasts (HLF-1) were investigated in vitro, and on bleomycin (BLM)-induced pulmonary fibrosis was investigated in vivo.

Results: In TGF-β1 stimulated A549 cells, treatment with GA resulted in a reduction of EMT with a decrease in vimentin and p-Smad3 and an increase in E-cadherin instead. In TGF-β1 stimulated HPMECs, treatment with GA resulted in a reduction of EndoMT with a decrease in vimentin, and an increase in VE-cadherin instead. In the hypoxic HPMECs, treatment with GA reduced Vasohibin-2 (VASH-2), whereas increased VASH-1. In TGF-β1 stimulated HLF-1, treatment with GA reduced HLF-1 proliferation with a decrease in platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF-2) expressions. In vivo, treatment with GA for 2 weeks resulted in an amelioration of the BLM-induced pulmonary fibrosis in rats with a lower VASH-2. Instead, it was observed a higher VASH-1 expression at early stage of fibrosis at 1 mg/kg, with reductions of the pathological score, collagen deposition, α-SMA, PDGF and FGF-2 expressions at fibrotic stage at 0.5 mg/kg and 1 mg/kg.

Conclusion: In summary, GA reversed EMT and EndoMT, as well as HLF-1 proliferation in vitro and prevented pulmonary fibrosis in vivo by modulating VASH-2/VASH-1 and suppressing the TGF-β1/Smad3 pathway.

Keywords: Gambogic acid; Pulmonary fibrosis; TGF-β1/Smad3; Vasohibin-1; Vasohibin-2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiogenic Proteins / metabolism
  • Animals
  • Bleomycin
  • Cadherins / metabolism
  • Cell Cycle Proteins / metabolism
  • Cell Proliferation / drug effects
  • Collagen / metabolism
  • Epithelial-Mesenchymal Transition / drug effects*
  • Fibroblast Growth Factor 2 / metabolism
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Fibrosis
  • Garcinia / chemistry*
  • Humans
  • Lung / drug effects*
  • Lung / metabolism
  • Lung / pathology
  • Male
  • Phytotherapy*
  • Plant Extracts / pharmacology
  • Plant Extracts / therapeutic use
  • Platelet-Derived Growth Factor / metabolism
  • Pulmonary Fibrosis / chemically induced
  • Pulmonary Fibrosis / drug therapy*
  • Pulmonary Fibrosis / metabolism
  • Pulmonary Fibrosis / pathology
  • Rats
  • Smad3 Protein / metabolism
  • Transforming Growth Factor beta1 / metabolism
  • Xanthones / pharmacology
  • Xanthones / therapeutic use*

Substances

  • Angiogenic Proteins
  • Cadherins
  • Cell Cycle Proteins
  • Plant Extracts
  • Platelet-Derived Growth Factor
  • Smad3 Protein
  • Smad3 protein, rat
  • Transforming Growth Factor beta1
  • VASH1 protein, human
  • VASH2 protein, human
  • Xanthones
  • Fibroblast Growth Factor 2
  • Bleomycin
  • gambogic acid
  • Collagen