摘要
OBJECTIVE: To investigate the effect of Pyunkanghwan(Pyunkang-tang) extract(PGT) on secretion of airway mucin in an experimental animal model involving hyperplasia of goblet cells and mucus hypersecretion, and to test its effects on bleomycin(BLM)-induced pulmonary fibrosis in vivo.METHODS: The protective activity of orally administered PGT was assessed in two rat pulmonary disease models. Effects on hypersecretion of pulmonary mucin in sulfur dioxide(SO_2)-induced bronchitis in rats were assessed by quantifying the amount of mucus secreted and examining histopathology in the tracheal epithelium. In a rat model for BLMinduced pulmonary fibrosis, toxicity to the pulmonary system was examined by measuring levels of malondialdehyde and hydroxyproline,indicators of lipid peroxides and collagen,respectively, in lung tissue 28 days post-BLM treatment. Serial sections of lung tissue were stained with Masson trichrome to visualize collagen deposition. Effects of PGT on collagen synthesis were also assessed in vitro, in a cell culture model.RESULTS: PGT inhibited mucin secretion and normalized SO_2-induced increased muco- substances in goblet cells. In the BLM- induced model,PGT decreased the characteristic histopathological features of lung fibrosis and inhibited fibrotic lesions, as indicated by decreased hydroxyproline content. PGT also inhibited the BLM-induced increase in malondialdehyde levels, demonstrating its protective effect against lipid peroxidation in cell membranes of the lung. In MLg 2908 mouse lung fibroblast cells, PGT decreased transforming growth factor(TGF)-β-stimulated type I collagen synthesis.CONCLUSION: PGT can inhibit both hypersecretion of airway mucins and pulmonary fibrosis.
OBJECTIVE： To investigate the effect of Pyunkanghwan（Pyunkang-tang） extract（PGT） on secretion of airway mucin in an experimental animal model involving hyperplasia of goblet cells and mucus hypersecretion, and to test its effects on bleomycin（BLM）-induced pulmonary fibrosis in vivo.METHODS： The protective activity of orally administered PGT was assessed in two rat pulmonary disease models. Effects on hypersecretion of pulmonary mucin in sulfur dioxide（SO_2）-induced bronchitis in rats were assessed by quantifying the amount of mucus secreted and examining histopathology in the tracheal epithelium. In a rat model for BLMinduced pulmonary fibrosis, toxicity to the pulmonary system was examined by measuring levels of malondialdehyde and hydroxyproline,indicators of lipid peroxides and collagen,respectively, in lung tissue 28 days post-BLM treatment. Serial sections of lung tissue were stained with Masson trichrome to visualize collagen deposition. Effects of PGT on collagen synthesis were also assessed in vitro, in a cell culture model.RESULTS： PGT inhibited mucin secretion and normalized SO_2-induced increased muco- substances in goblet cells. In the BLM- induced model,PGT decreased the characteristic histopathological features of lung fibrosis and inhibited fibrotic lesions, as indicated by decreased hydroxyproline content. PGT also inhibited the BLM-induced increase in malondialdehyde levels, demonstrating its protective effect against lipid peroxidation in cell membranes of the lung. In MLg 2908 mouse lung fibroblast cells, PGT decreased transforming growth factor（TGF）-β-stimulated type I collagen synthesis.CONCLUSION： PGT can inhibit both hypersecretion of airway mucins and pulmonary fibrosis.
