The anti-inflammatory and antibacterial mechanisms of bone marrow mesenchymal stem cells(MSCs) ameliorating lung injury in chronic obstructive pulmonary disease(COPD) mice induced by cigarette smoke and Haemophilus Pa...The anti-inflammatory and antibacterial mechanisms of bone marrow mesenchymal stem cells(MSCs) ameliorating lung injury in chronic obstructive pulmonary disease(COPD) mice induced by cigarette smoke and Haemophilus Parainfluenza(HPi) were studied. The experiment was divided into four groups in vivo: control group, COPD group, COPD+HPi group, and COPD+HPi+MSCs group. The indexes of emphysematous changes, inflammatory reaction and lung injury score, and antibacterial effects were evaluated in all groups. As compared with control group, emphysematous changes were significantly aggravated in COPD group, COPD+HPi group and COPD+HPi+MSCs group(P<0.01), the expression of necrosis factor-kappa B(NF-κB) signal pathway and proinflammatory cytokines in bronchoalveolar lavage fluid(BALF) were increased(P<0.01), and the phagocytic activity of alveolar macrophages was downregulated(P<0.01). As compared with COPD group, lung injury score, inflammatory cells and proinflammatory cytokines were significantly increased in the BALF of COPD+HPi group and COPD+HPi+MSCs group(P<0.01). As compared with COPD+HPi group, the expression of tumor necrosis factor-α stimulated protein/gene 6(TSG-6) was increased, the NF-κB signal pathway was depressed, proinflammatory cytokine was significantly reduced, the anti-inflammatory cytokine IL-10 was increased, and lung injury score was significantly reduced in COPD+HPi+MSCs group. Meanwhile, the phagocytic activity of alveolar macrophages was significantly enhanced and bacterial counts in the lung were decreased. The results indicated cigarette smoke caused emphysematous changes in mice and the phagocytic activity of alveolar macrophages was decreased. The lung injury of acute exacerbation of COPD mice induced by cigarette smoke and HPi was alleviated through MSCs transplantation, which may be attributed to the fact that MSCs could promote macrophages into anti-inflammatory phenotype through secreting TSG-6, inhibit NF-кB signaling pathway, and reduce inflammatory response through reducing proin展开更多
The aim of this study was to investigate the inhibitory effect of Cnidium monnieri fruit(CM) extracts on pulmonary inflammation induced in mice by cigarette smoke condensate(CSC) and lipopolysaccharide(LPS). Pulmonary...The aim of this study was to investigate the inhibitory effect of Cnidium monnieri fruit(CM) extracts on pulmonary inflammation induced in mice by cigarette smoke condensate(CSC) and lipopolysaccharide(LPS). Pulmonary inflammation was induced by intratracheal instillation of LPS and CSC five times within 12 days. CM extract was administered orally at a dose of 50 or 200 mg·kg-1. The number of inflammatory cells in the bronchoalveolar lavage fluid was counted using a fluorescence activated cell sorter. Inflammatory mediator levels were determined by enzyme-linked immunosorbent assay. The administration of LPS and CSC exacerbated airway hyper-responsiveness(AHR) and induced an accumulation of inflammatory cells and mediators, and led to histological changes. However, these responses are modulated by treatment with CM, and the treatment with CM extract produces similar or more extensive results than the treatment with cyclosporin A(CSA). CM extract may have an inhibitory effect on pulmonary inflammation related with chronic obstructive pulmonary disease.展开更多
基金supported by Medical Research of Henan Province(No.102300410247)
文摘The anti-inflammatory and antibacterial mechanisms of bone marrow mesenchymal stem cells(MSCs) ameliorating lung injury in chronic obstructive pulmonary disease(COPD) mice induced by cigarette smoke and Haemophilus Parainfluenza(HPi) were studied. The experiment was divided into four groups in vivo: control group, COPD group, COPD+HPi group, and COPD+HPi+MSCs group. The indexes of emphysematous changes, inflammatory reaction and lung injury score, and antibacterial effects were evaluated in all groups. As compared with control group, emphysematous changes were significantly aggravated in COPD group, COPD+HPi group and COPD+HPi+MSCs group(P<0.01), the expression of necrosis factor-kappa B(NF-κB) signal pathway and proinflammatory cytokines in bronchoalveolar lavage fluid(BALF) were increased(P<0.01), and the phagocytic activity of alveolar macrophages was downregulated(P<0.01). As compared with COPD group, lung injury score, inflammatory cells and proinflammatory cytokines were significantly increased in the BALF of COPD+HPi group and COPD+HPi+MSCs group(P<0.01). As compared with COPD+HPi group, the expression of tumor necrosis factor-α stimulated protein/gene 6(TSG-6) was increased, the NF-κB signal pathway was depressed, proinflammatory cytokine was significantly reduced, the anti-inflammatory cytokine IL-10 was increased, and lung injury score was significantly reduced in COPD+HPi+MSCs group. Meanwhile, the phagocytic activity of alveolar macrophages was significantly enhanced and bacterial counts in the lung were decreased. The results indicated cigarette smoke caused emphysematous changes in mice and the phagocytic activity of alveolar macrophages was decreased. The lung injury of acute exacerbation of COPD mice induced by cigarette smoke and HPi was alleviated through MSCs transplantation, which may be attributed to the fact that MSCs could promote macrophages into anti-inflammatory phenotype through secreting TSG-6, inhibit NF-кB signaling pathway, and reduce inflammatory response through reducing proin
基金supported by a grant under the National“973”program(No.2014CB932000) the Strategic Priority Research Program of the Chinese Academy of Sciences(No.XDB14000000)+2 种基金 grants from the National Natural Science Foundation of China(Nos.21425731 and 21637004) National Science Foundation No.CBET-1604119(Yi Y.Zuo) the Leahi Fund to Treat&Prevent Pulmonary Diseases#16ADVC-78729 from the Hawaii Community Foundation(Yi Y.Zuo)
文摘The aim of this study was to investigate the inhibitory effect of Cnidium monnieri fruit(CM) extracts on pulmonary inflammation induced in mice by cigarette smoke condensate(CSC) and lipopolysaccharide(LPS). Pulmonary inflammation was induced by intratracheal instillation of LPS and CSC five times within 12 days. CM extract was administered orally at a dose of 50 or 200 mg·kg-1. The number of inflammatory cells in the bronchoalveolar lavage fluid was counted using a fluorescence activated cell sorter. Inflammatory mediator levels were determined by enzyme-linked immunosorbent assay. The administration of LPS and CSC exacerbated airway hyper-responsiveness(AHR) and induced an accumulation of inflammatory cells and mediators, and led to histological changes. However, these responses are modulated by treatment with CM, and the treatment with CM extract produces similar or more extensive results than the treatment with cyclosporin A(CSA). CM extract may have an inhibitory effect on pulmonary inflammation related with chronic obstructive pulmonary disease.