Jinwei Tang modulates HDAC2 expression in a rat model of COPD

Wu,Jianjun; Li,Xin; Qin,Yang; Cheng,Juan; Hao,Gaimei; Jin,Ruifeng; Zhu,Chenjun

doi:10.3892/etm.2018.5707

Jinwei Tang modulates HDAC2 expression in a rat model of COPD

Authors:
- Jianjun Wu
- Xin Li
- Yang Qin
- Juan Cheng
- Gaimei Hao
- Ruifeng Jin
- Chenjun Zhu
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Affiliations: Department of Respiratory Disease, The Third Affiliated Hospital of Beijing University of Traditional Chinese Medicine, Beijing 100029, P.R. China, Department of Ocular Diseases, Eye Hospital, China Academy of Chinese Medical Sciences, Beijing 100040, P.R. China, Department of Pathology, Dongzhimen Hospital Affiliated to Beijing University of Traditional Chinese Medicine, Beijing 100700, P.R. China, Department of Pathology, Beijing University of Traditional Chinese Medicine, Beijing 100029, P.R. China, Department of Encephalopathy, The Third Affiliated Hospital of Beijing University of Traditional Chinese Medicine, Beijing 100029, P.R. China
Published online on: January 5, 2018 https://doi.org/10.3892/etm.2018.5707
Pages: 2604-2610

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Abstract

The aim of the present study was to investigate the effect of a Traditional Chinese Herbal Medicine (TCHM), named Jinwei Tang on histone deacetylase 2 (HDAC2) and its role in the regulation of corticosteroid resistance in a rat model of chronic obstructive pulmonary disease (COPD). Male Wistar rats were divided into five groups (each n=10): COPD group, established by the intratracheal instillation of lipopolysaccharide and passive smoke exposure, and control, budesonide, theophylline + budesonide and Jinwei Tang + budesonide groups. Lung function was measured, lung tissue histopathology was examined and HDAC2 expression in the lung was assessed by immunohistochemistry. In addition, protein levels of interleukin‑8 (IL‑8), tumor necrosis factor (TNF)‑α and HDAC2 in lung homogenate were quantified by ELISA. The rat COPD model exhibited alterations of the ratio of forced expiratory volume in 0.2 sec (FEV0.2) to the forced vital capacity, FEV0.2, dynamic compliance and airway resistance. HDAC2 expression was markedly reduced in the lung tissue of the COPD group compared with the control group, and treatment with Jinwei Tang + budesonide or theophylline + budesonide resulted in significant attenuation of the reduction of HDAC2 expression in the lungs (P<0.05). However, treatment with budesonide alone did not significantly alter HDAC2 expression. In the Jinwei Tang + budesonide and theophylline + budesonide groups, IL‑8 and TNF‑α expression was significantly decreased (P<0.05) and the HDAC2 level increased (P<0.05) compared with that in the COPD group. In conclusion, Jinwei Tang modulates airway inflammation and may enhance the anti‑inflammatory effect of glucocorticoid through the upregulation of HADC2 expression in a rat model of COPD.

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