Details

Autor(en) / Beteiligte

• Pan, Ruiyan
• Zhang, Yadan
• Zang, Baoxia
• Tan, Li
• Jin, Ming

Titel

Hydroxysafflor yellow A inhibits TGF-[beta]1-induced activation of human fetal lung fibroblasts in vitro

Ist Teil von

• Journal of pharmacy and pharmacology, 2016-10, Vol.68 (10), p.1320

Ort / Verlag

Bognor Regis: Wiley Subscription Services, Inc

Erscheinungsjahr

2016

Quelle

Wiley Online Library - AutoHoldings Journals

Beschreibungen/Notizen

• Objective Hydroxysafflor yellow A (HSYA) is one of the chemical component isolated from Chinese medicine Carthamus tinctorius L. Our preliminary study confirmed that HSYA attenuated bleomycin-induced pulmonary fibrosis in mice. In this study, we evaluated the effect of HSYA on TGF-[beta]1-induced activation of human fetal lung fibroblasts (MRC-5) and explored the underlying mechanisms of its activity. Method MRC-5 cells activated by TGF-[beta]1 were incubated with HSYA and/or the TGF-[beta] type I receptor inhibitor, SB431542. TGF-[beta]1-induced cell proliferation, [alpha]-smooth muscle actin, collagen I alpha 1 and fibronectin expression, Smad, mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3 kinase/Akt signalling pathway activation were observed. Key findings Hydroxysafflor yellow A significantly inhibited TGF-[beta]1-induced cell proliferation and the expression, both mRNA and protein, of [alpha]-smooth muscle actin, collagen I alpha 1 and fibronectin. HSYA also suppressed TGF-[beta]1 activation of Smad signal transduction via inhibition of Smad2 and Smad3 phosphorylation, their nuclear translocation and the binding activity of Smad3 to type I collagen promoter in MRC-5 cells. In addition, HSYA inhibited TGF-[beta]1-induced phosphorylation of extracellular signal-regulated kinase (ERK). The inhibitory effects of HSYA were similar to SB431542. Conclusion These findings suggest that HSYA inhibits TGF-[beta]1-induced activation of MRC-5 cells associated with TGF-[beta]1/Smad and ERK/MAPK signalling pathways.