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Evid Based Complement Alternat Med. 2014;2014:381976. doi: 10.1155/2014/381976. Epub 2014 May 14.

Effects and mechanism of bufei yishen formula in a rat chronic obstructive pulmonary disease model.

Evidence-based complementary and alternative medicine : eCAM

Jiansheng Li, Liping Yang, Qin Yao, Ya Li, Yange Tian, Suyun Li, Suli Jiang, Ying Wang, Xinmin Li, Zheng Guo

Affiliations

  1. Henan University of Traditional Chinese Medicine, Zhengzhou 450008, China.
  2. College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
  3. Respiratory Disease Institute, The First Affiliated Hospital of Henan University of TCM, Zhengzhou 450000, China.
  4. College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China ; Bioinformatics Centre, School of Life Science, University of Electronic Science and Technology of China, Chengdu 610054, China.

PMID: 24959185 PMCID: PMC4052073 DOI: 10.1155/2014/381976

Abstract

Bufei Yishen Formula (BYF) has been used for centuries in Asia to effectively treat patients with chronic obstructive pulmonary disease (COPD). This study established a COPD animal model in rats, wherein three groups (control, COPD, and BYF) were used to evaluate the mechanism(s) and curative effect of BYF. Pulmonary function and histomorphology demonstrated that BYF had an evident effect on COPD. Gene microarray was then exploited to analyze the effects of BYF on COPD. ClueGO analysis of differentially expressed genes indicated that BYF improved COPD by regulating expression of interleukins, myosin filament assembly components, and mitochondrial electron transport-related molecules. Moreover, ELISA revealed that expression of several interleukins (IL1 β , IL6, IL8, and IL10) was reduced in peripheral blood and bronchoalveolar lavage fluid by BYF treatment. It was concluded that BYF has therapeutic effects on COPD in rats through its effects on interleukin expression and/or secretion. Furthermore, pharmacological or targeted expression of two differentially expressed genes,   F2R and    Sprik1, might be useful in novel COPD therapies. This study provides the basis for mechanisms of BYF on COPD and new therapeutic drug targets.

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