• Journal of Veterinary Clinics
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• v.33 no.5
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• pp.255-260
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• 2016

$Pyunkang-tang^{(R)}$ is a kind of herbal medicine and has been used for the treatment of atopy and allergic disease in humans over forty years. The purpose of this study was to evaluate the hematological, biochemical, and protein and lipid electrophoresis profiles after the oral administration of $Pyunkang-tang^{(R)}$ in healthy dogs. Fifteen clinically healthy beagle dogs were selected and orally administered either 33 ml of $Pyunkang-tang^{(R)}$ (group I, n = 5), 16.5 ml of $Pyunkang-tang^{(R)}$ (group II, n = 5), or 33 ml of distilled water (group III, n = 5) 3 times a day for 4 weeks. The results of the hematological, serum biochemical, and urine analysis did not differ significantly among the 3 groups. The oral administration of $Pyunkang-tang^{(R)}$ for 4 weeks was associated with significant changes in the serum globulin levels and an elevation in the high-density lipoprotein (HDL) concentrations in groups I and II (p < 0.05), compared to group III. The ${\alpha}1-globulin$ and ${\gamma}-globulin$ levels were significantly increased in group I, and the ${\alpha}1-globulin$ and ${\beta}-globulin$ levels were significantly increased in group II. The ${\alpha}2-globulin$ levels were significantly decreased in both groups. During the short-term evaluation of $Pyunkang-tang^{(R)}$ administration, we did not detect any specific adverse effects in the dogs. However, further evaluation of the safety and efficacy of $Pyunkang-tang^{(R)}$ for the treatment of atopic disease in dogs is needed.

• Natural Product Sciences
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• v.20 no.3
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• pp.196-201
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• 2014

Pyunkang-hwan (Pyunkang-tang) extract (PGT) is a traditional folk medicine for controlling diverse pulmonary diseases including bronchitis, tonsiltis and pneumonitis. We investigated whether PGT significantly affects secretion, production and gene expression of airway mucin using in vivo and in vitro experimental models reflecting the hypersecretion and/or hyperproduction of mucus observed in inflammatory pulmonary diseases. For in vivo experiment, effect of PGT was checked on hypersecretion of pulmonary mucin in sulfur dioxide-induced bronchitis in rats. For in vitro experiment, confluent NCI-H292 cells were pretreated with PGT for 30 min and then stimulated with EGF (epidermal growth factor), PMA (phorbol 12-myristate 13-acetate) or TNF-${\alpha}$ (tumor necrosis factor-${\alpha}$) for 24 h. The MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. The results were as follows: (1) PGT inhibited the expression of MUC5AC mucin gene induced by EGF, PMA or TNF-${\alpha}$ from NCI-H292 cells, respectively; (2) PGT also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI-H292 cells, respectively; (3) PGT inhibited secretion of mucin in sulfur dioxide-induced bronchitis rat model. This result suggests that PGT can regulate secretion, production and gene expression of airway mucin.

• Natural Product Sciences
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• v.25 no.2
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• pp.103-110
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• 2019

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-${\alpha}$ (TNF-${\alpha}$) 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-${\alpha}$ 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.