| RESEARCH ARTICLE |
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| Year : 2019 | Volume
: 51
| Issue : 4 | Page : 263-268 |
Jian-Pi-Yi-Fei granule suppresses airway inflammation in mice induced by cigarette smoke condensate and lipopolysaccharide
Cui-Ying Tang1, Si-Li Tang2, Kai-Feng Huang1, Jian Xu1, Hui Yu1, Lin Lin1
1 Department of Respiratory, Guangdong Hospital of Traditional Chinese Medicine, Guangzhou, China
2 Department of Pharmacochemistry, College of Pharmaceutical Science, Guangzhou Medical University, Guangzhou, China
Correspondence Address:
Dr. Lin Lin
Department of Respiratory, Guangdong Hospital of Traditional Chinese Medicine, 111 Dade Road, Guangzhou, 510120
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijp.IJP_105_18
INTRODUCTION: As a chronic, progressive, and lethal pulmonary disease, chronic obstructive pulmonary disease (COPD) is lacking effective treatment. Chronic inflammatory processes, including inflammatory cytokines, play an important role with in its pathogenesis. Jianpiyifei (JPYF) granule is a traditional Chinese herbal formula historically used to strengthen the spleen and tonify the lung. JPYF is used clinically to treat stable COPD. However, whether the purported anti-inflammatory effect of JPYF in COPD involves regulation of key inflammatory cytokines is not clear.
MATERIALS AND METHODS: The mice model of pulmonary inflammation was induced by lipopolysaccharide (LPS) and cigarette smoke condensate (CSC). The influence of JPYF on airway inflammation in vivo was investigated. Mice were divided into three groups: control, model, and treatment groups. In the CSC + LPS model group and JPYF treatment group, intratracheal injection of CSC and LPS was used to induce airway inflammation for 5 days. JPYF group animals were also orally administered 5.5 g/kg JPYF granule for 12 days.
RESULTS: The number of neutrophils and total cells in bronchoalveolar lavage fluid of the JPYF group were markedly lower than in the model group. The levels of interleukin (IL)-1 β and IL-6 were lower; tumor necrosis factor-alpha was downregulated, and IL-10 was higher in the JPYF group than the model group. In the JPYF group, histone deacetylase 2 (HDAC2) activity and protein expression were restored.
CONCLUSION: The anti-inflammatory activity of JPYF involves the suppression of pro-inflammatory cytokines, enhanced IL-10 secretion, and the restoration of HDAC2 activity.
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