Open AccessSchisandrin B down‐regulated lnc RNA BCYRN 1 expression of airway smooth muscle cells by improving miR‐150 expression to inhibit the proliferation and migration of ASMC in asthmatic rats
Author(s) -
Zhang Xiaoyu,
Tang Xueyi,
Ma Lijun,
Guo Yali,
Li Xiaosu,
Zhao Limin,
Tian Cuijie,
Cheng DongJun,
Chen Zhuochang,
Zhang Luoxian
Publication year - 2017
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12382
Subject(s) - chemistry , messenger rna , transfection , viability assay , microbiology and biotechnology , rna , pharmacology , cell , biology , biochemistry , gene
Objective The mechanism of Schisandrin B on the proliferation and migration of airway smooth muscle cells (ASMCs) in asthmatic rats was explored. Methods SD rats were divided into three groups: control (group 1), model (group 2) and model + Schisandrin B (group 3). miR‐150 and lnc RNA BCYRN 1 levels were measured by qRT ‐ PCR . The combination of BCYRN 1 and miR‐150 was detected by RNA pull down. ASMCs’ viability/proliferation/migration were examined by WST ‐1 assay and 24‐well Transwell system. Results Schisandrin B up‐regulated miR‐150 expression and down‐regulated BCYRN 1 expression in sensitized rats. Schisandrin B reversed the expression of miR‐150 and BCYRN 1 in MV ‐treated ASMC s. In addition, Schisandrin B inhibited the viability, proliferation and migration of MV ‐induced ASMC s. We also found miR‐150 inhibited BCYRN 1 expression which was proved by experiments using ASMC s transfected with miR‐150 inhibitor. Conclusion Schisandrin B increased miR‐150 expression and decreased BCYRN 1, and BCYRN 1 expression was inhibited by miR‐150, which indicated that Schisandrin B could regulate BCYRN 1 through miR‐150.