Calcitriol Combined With Budesonide Inhibits the Secretion and Expression of IL-33 in Mouse Airway Smooth Muscle Cells
Abstract BackgroundBronchial asthma (asthma) is a chronic respiratory inflammatory disease characterized by reversible airflow limitation and high airway reactivity. Current studies generally show that airway remodeling is the pathologic structural basis for the occurrence of reversible airflow restriction and airway hyper reactivity[1] [2].In the above process, airway smooth muscle cell (ASMC) hyperplasia and hypertrophy are considered to be the main mechanisms of airway remodeling[3]. Calcitriol can be combined with budesonide to more effectively inhibit airway inflammation and airway remodeling and play its role in the treatment of asthma[4, 5]. MethodsThe mouse airway smooth muscle cells were divided into blank group, TGF-β1 group, SIS3 group, budesonide group,calcitriol group and drug co-treatment group[6]. The IL-33 concentration in supernatant of each group was detected by ELISA method, and the expression of Smad3, pSmad3 and IL-33 protein in each group was detected by Western blotting method[7].ResultsELISA showed that the concentration of IL-33 in the supernatant of cell culture in budesonide group was lower than that in the calcitriolgroup, and the concentration of IL-33 in the drugco-treatment group was lower than that in any single drugtreatment group.The expression level of Smad3 protein, pSmad3 protein and IL-33 protein of western blot in the drug co-treatment group were significantly decreased[8, 9].ConclusionsCalcitriol combined with budesonide can effectively decrease the expression and secretion of IL-33 in mouseairway smooth muscle cells byactivatingTGF-β1/Smad3 signaling pathway [10].