Open AccessBioactive molecule Icariin inhibited proliferation while enhanced apoptosis and autophagy of rat airway smooth muscle cells in vitro
Author(s) -
Lihong Yang,
Bo Xiao,
Lixia Hou,
Guangxi Zhou,
Biwen Mo,
Yao Dong
Publication year - 2019
Publication title -
cytotechnology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.488
H-Index - 62
eISSN - 1573-0778
pISSN - 0920-9069
DOI - 10.1007/s10616-019-00348-9
Subject(s) - icariin , autophagy , apoptosis , flow cytometry , tunel assay , microbiology and biotechnology , cell cycle , cell growth , chemistry , biology , biochemistry , medicine , pathology , alternative medicine
Icariin is the main active compound extracted from epimedium Flavonoids (EFs) and involved in regulation of cell behaviors (proliferation, apoptosis, and autophagy etc.) for many cell types, but the effect of Icariin on airway smooth muscle cells (ASMCs) is still unknown. The aim of the present study is to examine the role of Icariin on rat ASMCs proliferation, apoptosis and autophagy. CKK8 assay showed that Icariin inhibited rat ASMCs growth in dose-time-dependent manner, and the flow cytometry assay showed that the Icariin interfered with ASMCs cell cycle, when treated with Icariin, S phase shortened while G2 phase extended, cyclin E1 and cyclinA1 gene and protein expression decreased. Next apoptosis was detected, Flow cytometry and TdTmediated dUTP Nick-End Labeling (TUNEL) assay showed that Icariin promoted ASMCs apoptosis, and enhanced apoptosis protein cleaved-caspase-3 expression. Finally, it was found Icariin induced rat ASMCs autophagy, with enhancement expression of autophagy marker LC3 II. In conclusion, Icariin inhibited ASMCs proliferation while promoted apoptosis and autophagy, revealing its potential role in treatment of airway remodeling in asthma.