Effect of dioscin on glucocorticoid receptor of airway epithelial cells in mice with asthma

LI Xianqian; WU Ning; YU Ronghuan; GUAN Chao; XU Ting; WU Jiaxi

doi:10.3969/j.issn.1002-266X.2017.42.005

Abstract：Objective To observe the effects of dioscin on the glucocorticoid receptor GRα and GRβ of airway epithe-lial cells in mouse models with asthma,and to investigate its anti-inflammatory effect on asthma. Methods Normal mouse airway epithelial cells were used as the blank control group,and the airway epithelial cells from asthmatic mouse models were divided into 3 groups as following:asthmatic non-treatment group (cells cultured in a medium containing no drug), asthmatic treatment group (cells cultured in a medium containing dioscin),and asthmatic antagonistic group (cells cul-tured in medium containing dioscin and GR antagonists,RU486). The levels of IL-1,IL-6 and TNF-α in the conditional media were measured by using ELISA. The mRNA and protein levels of GRα,GRβ,and HSP90 in the cells were detected by using real-time quantitative PCR and Western blotting,respectively. Results The levels of IL-1,IL-6,and TNF-αwere significantly higher in the asthmatic non-treatment group than in the asthmatic treatment group and the blank control group,and the levels of IL-1,IL-6,and TNF-α were higher in the asthmatic antagonistic group than in the asthmatic treat-ment group (all P <0.05). The expression of GRα,GRβ,and HSP90 at protein and mRNA levels was significantly lower in the asthmatic treatment group than in the blank control group (all P<0.05). The expression of GRα was higher,while the expression of GRβ and HSP90 at protein and mRNA levels was lower in the asthmatic treatment group than in the asth-matic non-treatment group (all P < 0.05). The expression of GRα,GRβ,and HSP90 at protein and mRNA levels of the asthmatic antagonistic group had no statistic difference as compared with that of the asthmatic non-treatment group. Conclu-sion Dioscin exerts its anti-inflammatory effects in asthmatic mice by regulating the expression of GRα,GRβ,and HSP90 in airway epithelial cells.