Eur Rev Med Pharmacol Sci 2012; 16 (12): 1701-1706

Research on the molecular mechanism of Seretide treatment to asthma disease

Z.-W. Liu, F. Yue, F.-Y. Gao, Y.-B. Qian, R.-L. Wang

Department of Respiratory Medicine, First people’s Hospital affiliated to Shanghai Jiao Tong University, Shanghai, China. wangyusun@hotmail.com


INTRODUCTION: Asthma is one of the most common chronic diseases in children. It is attributable to complicated coactions between various genetic factors and environmental allergens.

AIM: We attempt to unfold the mechanism of asthmatic disorder and research the molecular mechanism of Seretide on asthmatic disease.

MATERIALS AND METHODS: Using the GSE31773 microarray datasets downloaded from Gene Expression Omnibus database, we first screened the differentially expressed genes between healthy control and asthmatic samples cells based on classical t-test and false discovery rate < 0.05 as significant threshold. The underlying molecular mechanisms were investigated by Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. In addition, the crosstalk network of pathways was also constructed.

RESULTS: A total of 2011 differentially expressed genes were obtained by comparing asthmatic sample treated with Seretide and healthy controls. A total of 403 differentially expressed genes were collected between asthma samples untreated by Seretide and healthy sample controls. The enriched pathway of differentially expressed genes included signal transduction disorder (such as TGF-beta signaling pathway) and metabolism disorder (such as Phenylalanine metabolism). There were 27 pathway crosstalk pairs among 13 pathways.

CONCLUSIONS: Our findings will help to clarify the molecular mechanism of Seretide and offer advices for asthma pathogenesis, Seretide therapy and follow-up treatment.

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To cite this article

Z.-W. Liu, F. Yue, F.-Y. Gao, Y.-B. Qian, R.-L. Wang
Research on the molecular mechanism of Seretide treatment to asthma disease

Eur Rev Med Pharmacol Sci
Year: 2012
Vol. 16 - N. 12
Pages: 1701-1706