Abstract
BuqiHuoxueTongluo Formula (BHTF) is an effective herbal prescription based on traditional Chinese medicine for idiopathic pulmonary fibrosis (IPF). The aim of this study was to elucidate the influence of BHTF on induced IPF model through the aspect of histopathology and pulmonary function test. Wistar rats with bleomycin-induced IPF were given BHTF via intragastric gavage. After 14 days and 28 days of treatment, respectively, on these two time points, we first performed pulmonary function test, performed ventilation measure, and traced the Pressure-Volume Loop under anesthesia. Then, rats were sacrificed for hematoxylin-eosin and Masson's trichrome staining, immunohistochemistry staining of TGF-β1 and α-SMA, and observation through transmission electron microscope. BHTF reduced infiltration of inflammation cells, collagen deposition, and fibrosis proliferation in pulmonary mesenchyme, inhibited the expression of TGF-β1 and α-SMA, and avoided the abnormality of ultrastructure and quantities of lamellar bodies. It also ameliorated the parameters of FVC, MVV, PEF, FEF25, and Cdyn, maintained the shape of the Pressure-Volume Loop, and improved hysteresis. BHFT relieved the histopathologic changes, improved ventilation function, compliance, and work of breathing, meliorated the capacity and elasticity of the lungs, and stabilized the alveolar surface tension. Further speaking, it had a potential impact on the secretion of pulmonary surfactant.
Highlights
Idiopathic pulmonary fibrosis (IPF) is a chronic, diffuse, progressive disease of the pulmonary interstitium with agnogenic etiology [1], and it lacks effective therapy in the clinic [2]
H&E staining of lung tissues was performed for observation of inflammation changes [21]
Compared with the BLM group, treatment with prednisone and BuqiHuoxueTongluo Formula (BHTF) could reduce the thickness of alveolar septa and infiltration of inflammation cells
Summary
Idiopathic pulmonary fibrosis (IPF) is a chronic, diffuse, progressive disease of the pulmonary interstitium with agnogenic etiology [1], and it lacks effective therapy in the clinic [2]. Transforming growth factor β1 (TGF-β1) was the most important starting factor of IPF [7]; it could accelerate the progress with which alveolar epithelial cell is transformed into mesenchymal myofibroblast, and its specific marker α-smooth muscle actin (α-SMA) was overexpressed [8]. During this course of epithelial-mesenchymal transition (EMT), the function of type II alveolar epithelial cell (AECII) such
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