Effect of Pyunkang-tang on Inflammatory Aspects of Chronic Obstructive Pulmonary Disease in a Rat Model
10.20307/nps.2019.25.2.103
- Author:
Hyo Seok SEO
1
;
Hyun Jae LEE
;
Choong Jae LEE
Author Information
1. Department of Pharmacology, School of Medicine, Chungnam National University, Daejeon, Korea. LCJ123@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
Pyunkang-tang;
COPD;
inflammation;
mucin
- MeSH:
Animals;
Bronchoalveolar Lavage Fluid;
Campanulaceae;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells;
Epithelium;
Gene Expression;
Goblet Cells;
Humans;
In Vitro Techniques;
Inflammation;
Inhalation;
Interleukin-6;
Korea;
Lonicera;
Lung Diseases;
Medicine, Chinese Traditional;
Models, Animal;
Mucins;
Mucus;
Necrosis;
Pathology;
Pneumonia;
Pulmonary Disease, Chronic Obstructive;
Rats;
Rehmannia;
Selaginellaceae;
Smoke;
Sulfur Dioxide;
Tobacco Products
- From:Natural Product Sciences
2019;25(2):103-110
- CountryRepublic of Korea
- Language:English
-
Abstract:
We investigated the anti-inflammatory effect of Pyunkang-tang extract (PGT), a complex herbal extract based on traditional Chinese medicine that is used in Korea for controlling diverse pulmonary diseases, on cigarette smoke-induced pulmonary pathology in a rat model of chronic obstructive pulmonary disease (COPD). The constituents of PGT were Lonicerae japonica, Liriope platyphylla, Adenophora triphilla, Xantium strumarinum, Selaginella tamariscina and Rehmannia glutinosa. Rats were exposed by inhalation to a mixture of cigarette smoke extract (CSE) and sulfur dioxide for three weeks to induce COPD-like pulmonary inflammation. PGT was administered orally to rats and pathological changes to the pulmonary system were examined in each group of animals through measurement of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels in bronchoalveolar lavage fluid (BALF) at 21 days post-CSE treatment. The effect of PGT on the hypersecretion of pulmonary mucin in rats was assessed by quantification of the amount of mucus secreted and by examining histopathologic changes in tracheal epithelium. Confluent NCI-H292 cells were pretreated with PGT for 30 min and then stimulated with CSE plus PMA (phorbol 12-myristate 13-acetate), for 24 h. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. The results were as follows: (1) PGT inhibited CSE-induced pulmonary inflammation as shown by decreased TNF-α and IL-6 levels in BALF; (2) PGT inhibited the hypersecretion of pulmonary mucin and normalized the increased amount of mucosubstances in goblet cells of the CSE-induced COPD rat model; (3) PGT inhibited CSE-induced MUC5AC mucin production and gene expression in vitro in NCI-H292 cells, a human airway epithelial cell line. These results suggest that PGT might regulate the inflammatory aspects of COPD in a rat model.
