Research Article

Qingfei Tongluo Mixture Attenuates Bleomycin-Induced Pulmonary Inflammation and Fibrosis through mTOR-Dependent Autophagy in Rats

Figure 3

QFTL inhibits bleomycin-induced fibrosis progression. (a) Results of H&E staining showed that QFTL reduced inflammatory damage in rats with bleomycin-induced pulmonary fibrosis. In the control group, the lung tissue structure was normal, with no obvious morphological or pathological changes observed; in the model group, extensive thickening of the alveolar walls was observed in lung tissue, accompanied by a large amount of infiltration of inflammatory cells (black arrow), extensive proliferation of connective tissue (brown arrow), and localized bronchial hyperplasia. The proliferative bronchial lumen was filled with macrophages (blue arrow) and a large number of bronchial epithelial cells were necrotic and shed. A large number of necrotic cell fragments and inflammatory cells (red arrow) were visible in the lumen; in the CQ + QFTL group, extensive thickening of the alveolar walls was observed in lung tissue, accompanied by excessive infiltration of inflammatory cells (black arrow) and a small amount of connective tissue hyperplasia (brown arrow). Bronchial mucosal epithelial cells were necrotic and disappeared, and a large number of inflammatory cells were observed in the lumen (red arrow). In the QFTL-L group, focal connective tissue hyperplasia (brown arrow) can be seen on the alveolar wall in multiple locations of lung tissue, with a significant amount of inflammatory cell infiltration (black arrow). A large number of bronchial mucosal epithelial cells are necrotic and shed, and a large number of necrotic cell fragments (yellow arrow) and inflammatory cells (red arrow) can be seen in the lumen; in the QFTL-M group, focal thickening of the alveolar walls was observed in lung tissue, accompanied by a large amount of infiltration of inflammatory cells (black arrow). A large number of inflammatory cells were often observed in the lumen of the bronchi (red arrow), and local necrosis and disappearance of bronchial epithelial cells were observed (yellow arrow); in the QFTL-H group, a small area of thickening of the alveolar wall was observed in lung tissue, accompanied by a large amount of infiltration of inflammatory cells (black arrow) and a small amount of connective tissue proliferation (brown arrow). There was no obvious shedding of bronchial mucosal epithelial cells, and a large amount of dead debris and inflammatory cells (red arrow) were visible in the lumen of the bronchi. In the PFD group, focal thickening of the alveolar wall was observed in lung tissue, accompanied by a large amount of infiltration of inflammatory cells (black arrow), a small amount of proliferation of connective tissue (brown arrow), a large number of inflammatory cells were observed in the lumen of the bronchi (red arrow), local bronchial proliferation was observed and a small number of inflammatory cells were observed in the proliferative bronchial lumen (red arrow). The arrow indicates the injury area. (b) Representative photomicrographs of rat lung tissues stained with Masson’s trichrome. Blue staining indicated collagen deposition. (c) Quantitative assessment of pulmonary fibrosis, as measured by Ashcroft histopathological scoring. After examining the entire section, the mean score of all the fields was taken as the fibrosis score for the section. The higher score indicated the severe fibrosis. (d) Quantitative evaluations of collagen deposition in Massion-stained lung tissue were performed using automated image analysis software (Image-Pro Plus). (e) Quantitative evaluations of hydroxyproline were measured in different treatment groups using HYP assay kit. Data presented are means ± SD. vs. control; # vs. model; Δ vs. PFD.
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