Objective To investigate the effect of atomization inhalation of budesonide and terbutaline sulfate on serum levels of cyclcoxygenase 2 (COX-2) and chemokine like factor-1 (CKLF-1) in children with bronchial asthma.Methods A total of 78 children with bronchial asthma in Hangzhou Children's Hospital from April 2016 to August 2017 were selected and divided into the control group(n =39) and the study group(n =39).The control group was treated with routine treatment,and the study group was treated with budesonide and terbutaline sulfate on the basis of the control group.The treatment was continued for 7 d.After t treatment,the clinical effects,clinical symptoms improvement,hospitalization time,the serum levels of COX-2 and CKLF-1 before and after treatment,and the incidence of adverse reaction of two groups were observed.Results The total effective rate of the study group(94.87％) was higher than that of the control group (74.36％)(x2 =6.303,P ＜ 0.05).The improvement time of chest tightness,wheezing,cough and hospitalization time of the study group were shorter than those of the control group (t1 =13.054,t2 =7.365,t3 =4.944,t4 =8.342,all P ＜ 0.05).After treatment,the levels of serum COX-2 and CKLF-1 in the two groups were lower than those before treatment,which of the study group were lower than those in the control group(t1 =4.934,t2 =4.660,all P ＜0.05).There was statistically significant difference in the incidence rate of adverse reactions between the study group(12.82％) and the control group(7.69％) (x2 =0.139,P ＞ 0.05).Conclusion Atomization inhalation of budesonide and terbutaline sulfate in the treatment of children with bronchial asthma can effectively alleviate the clinical symptoms,reduce serum levels of COX-2 and CKLF-1,improve therapeutic effect,promote children's recovery and shorten the hospitalization time.Besides,the incidence rate of adverse reactions is low,and it is safe.

Purpose: Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. Materials and Methods: We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. Results: SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. Conclusion These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.

Purpose: Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. Materials and Methods: We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. Results: SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. Conclusion These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.