4.3 Article

Protective Effect of Ginsenoside Rg1 on Bleomycin-Induced Pulmonary Fibrosis in Rats: Involvement of Caveolin-1 and TGF-β1 Signal Pathway

Journal

BIOLOGICAL & PHARMACEUTICAL BULLETIN
Volume 39, Issue 8, Pages 1284-1292

Publisher

PHARMACEUTICAL SOC JAPAN
DOI: 10.1248/bpb.b16-00046

Keywords

Ginsenoside Rg1; pulmonary fibrosis; hydroxyproline; alpha smooth muscle actin; Caveolin-1; transforming growth factor-beta 1

Funding

  1. National Natural Science Foundation of China [81470510, 81170597]
  2. Xinxiang Science and Technology Key Projects Fund, Henan, China [S10008]

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Idiopathic pulmonary fibrosis (IPF) is a progressive disease with poor prognosis and high mortality rate. Panax Notoginseng Saponins (PNS), extracted from Panax Notoginseng as a traditional Asian medicine, displayed a significant anti-fibrosis effect in liver and lung. However, whether Ginsenoside Rg1 (Rg1), an important and active ingredient of PNS, exerts anti-fibrotic activity on IPF still remain unclear. In this study, we investigated the effect of Rg1 on bleomycin-induced pulmonary fibrosis in rats. Bleomycin (5 mg/kg body weight) was intratracheally administrated to male rats. Rg1 (18, 36 and 72 mg/kg) was orally administered on the next day after bleomycin. Lungs were harvested at day 7 and 28 for the further experiments. Histological analysis revealed that bleomycin successfully induced pulmonary fibrosis, and that Rg1 restored the histological alteration of bleomycin-induced pulmonary fibrosis (PF), significantly decreased lung coefficient, scores of alveolitis, scores of PF as well as contents of alpha smooth muscle actin (alpha-SMA) and hydroxyproline (Hyp) in a dose-dependent manner in PF rats. Moreover, Rg1 increased the expression levels of Caveolin-1 (Cav-1) mRNA and protein, lowered the expression of transforming growth factor-beta (TGF-beta 1) mRNA and protein in the lung tissues of PF rats. These data suggest that Rgl exhibits protective effect against bleomycin-induced PF in rats, which is potentially associated with the down-regulation of TGF-beta 1 and up regulation of Cav-1.

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