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Salidroside inhibits platelet‐derived growth factor–induced proliferation and migration of airway smooth muscle cells
Author(s) -
Li Hong,
Yang Tian,
Wu Rui,
Chen Tianjun,
Sun Zhongmin,
Yang Lan
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27960
Subject(s) - salidroside , platelet derived growth factor , microbiology and biotechnology , airway , growth factor , chemistry , smooth muscle , transforming growth factor , platelet derived growth factor receptor , endocrinology , biology , medicine , biochemistry , anesthesia , receptor , chromatography
Abnormal proliferation and migration of airway smooth muscle cells (ASMCs) have been found to be important for the airway remodeling during the pathogenesis of asthma. Salidroside a bioactive glucoside that exerts antitumor activity via inhibiting the cell proliferation and migration of cancer cells. The aim of the current study was to evaluate the effects of salidroside on the proliferation and migration of ASMCs. Our results showed that salidroside inhibited the proliferation and migration of ASMCs in response to platelet‐derived growth factor (PDGF) stimulation. Salidroside markedly attenuated the PDGF‐induced production of matrix metalloproteinase 2 (MMP‐2) and MMP‐9 in ASMCs. The levels of contractile phenotype markers including smooth muscle α‐actin and calponin were reduced in response to PDGF stimulation, which was attenuated by salidroside pretreatment. Salidroside diminished the increase in the expression levels of type I collagen and fibronectin in PDGF‐stimulated ASMCs. Furthermore, salidroside blocked the PDGF‐induced activation of the nuclear factor‐κB (NF‐κB) pathway in ASMCs. The results suggested that salidroside functionally regulated the proliferation, migration, phenotype plasticity, and extracellular matrix deposition in PDGF‐induced ASMCs and the NF‐κB pathway might be implicated in the effects of salidroside on ASMCs induced by PDGF.