Objective. To investigate the intervention effect and functioning mechanismof citrus alkaline extract (CAE) on bleomycin- (BLM-)\ninduced pulmonary fibrosis in mice. Methods. 42 C57BL/6 male mice were assigned randomly to the normal group, model group,\nlow (16mg/kg), medial (32mg/kg) and high (64mg/kg) CAE dosage groups, prednisone group (6mg/kg), and pirfenidone group\n(100mg/kg), respectively. One day after model construction, intragastric administration was applied to the mice once a day for 28\ndays and then killed. Body weights of mice were recorded. Their pulmonary tissues were subjected to HE staining and Massonâ??s\nstaining and then their degree of pulmonary alveolitis as well as pulmonary fibrosis was scored. Contents of hydroxyproline (HYP)\nand prostaglandin E2 (PGE2) in pulmonary tissues and levels of interleukin-17 (IL-17) in serum and bronchoalveolar lavage fluid\n(BALF) were determined by ELISA method. Expression of collagen I, collagen III, and Prosurfactant protein C (Pro-SPC) proteins\nin pulmonary tissue weremeasured immunohistochemically and that of nuclear transcription factor kB (NF-kB) and vimentin was\ndetermined by the immunofluorescence method.Apoptosis of pulmonary tissue was tested by the Tunel stainingmethod, while the\nexpression ofMAPK-relatedproteinwas recorded byWestern Blot assay. Results.AfterCAE treatment, the bodyweight, PGE2 level,\nand Pro-SPC protein expression of pulmonary fibrosismice were increased, while the score of pulmonary alveolitis and pulmonary\nfibrosis, levels of HYP and cell apoptosis, IL-17 contents of serum and BALF in pulmonary tissues, and expression of collagen\nI, collagen III, vimentin, NF-kB, and p-p38 were reduced. Conclusion. CAE effectively delayed the progression of BLM-induced\npulmonary fibrosis in pulmonary fibrosis mice and a possiblemechanismis the inhibition of cell apoptosis of NF-kB/p38-mediated\nsignaling pathway kB (NF-kB) and vimentin was\ndetermined by the immunofluorescence method.Apoptosis of pulmonary tissue was tested by the Tunel stainingmethod, while the\nexpression ofMAPK-relatedproteinwas recorded byWestern Blot assay. Results.AfterCAE treatment, the bodyweight, PGE2 level,\nand Pro-SPC protein expression of pulmonary fibrosismice were increased, while the score of pulmonary alveolitis and pulmonary\nfibrosis, levels of HYP and cell apoptosis, IL-17 contents of serum and BALF in pulmonary tissues, and expression of collagen\nI, collagen III, vimentin, NF-kB, and p-p38 were reduced. Conclusion. CAE effectively delayed the progression of BLM-induced\npulmonary fibrosis in pulmonary fibrosis mice and a possiblemechanismis the inhibition of cell apoptosis of NF-kB/p38-mediated\nsignaling pathway
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