Experimental lung research
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Idiopathic interstitial pneumonias (IIPs) are a group of diffuse parenchymal lung diseases of unknown etiology characterized by the presence of various degrees of inflammation and fibrosis. We aimed to screen the differences among IIPs subtypes in the gene level by using the microarray expression profiles of normal lung tissue and IIPs tissue for the key genes associated with early diagnosis and treatment of IIPs. ⋯ This comprehensive description of altered gene expression in different subtypes of IIPs underscores the complex biological processes characteristic of different subtypes of IIPs and may provide a foundation for future research into this devastating disease.
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Angiogenesis is a central component of normal wound healing but it has not been fully characterized in lung repair following acute inflammatory injury. The current literature lacks vital information pertaining to the extent, timing, and location of this process. This information is necessary for examining mechanisms that drive normal lung repair in resolving acute inflammatory injury. The goal of our study was to formally characterize lung angiogenesis over a time course of bleomycin-induced lung injury. ⋯ Angiogenesis begins shortly after injury in the bleomycin model and leads to an expansion in the lung endothelial cell population that peaks at day 21. This study offers the first longitudinal examination of angiogenesis following acute inflammatory lung injury induced by bleomycin. Information provided in this study will be vital for further investigating mechanisms of angiogenesis in both normal and abnormal lung repair.
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Chronic obstructive pulmonary disease is an inflammatory lung disease mainly caused by tobacco smoke inhalation. ⋯ Cigarette smoke increases airway responsiveness and inflammation in a cat model of CS induced lung inflammation. It can effectively be reduced by treatment with tiotropium.
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Recent studies have demonstrated that peroxisome proliferator-activated receptor-beta/delta (PPAR-β/δ) has a protective effect during lung injury induced by bleomycin and polymicrobial sepsis, but its function in pulmonary oxygen toxicity is unknown. In this study, we used GW0742, a PPAR-β/δ agonist, and GSK0660, a PPAR-β/δ antagonist, to test the role of PPAR-β/δ in lung injury due to hyperbaric oxygen (HBO2) exposure. Lung injury was induced in rats by HBO2 exposure (2.3 ATA, 100%O2, 8 hours). ⋯ In addition, nNOS and eNOS knock-out mice were examined. The results indicated that after HBO2 exposure, the lung injury was obviously decreased in the nNOS(-/-)+GSK0660 mice compared to the wild-type +GSK0660 mice; furthermore, administration of GSK0660 significantly elevated the lung injury in the eNOS(-/-) mice. Collectively, these data indicate that PPAR-β/δ activation can protect against pulmonary oxygen toxicity in the lungs of rats through changes in the expression of NOS.
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Salvianolic acid B (Sal B), one of the major water-soluble compounds of Danshen (a popular Chinese herb), possesses many of the biological activities, such as antifibrogenic effect in liver and renal diseases. Transforming growth factor-β1 (TGF-β1) plays a central role in the development of pulmonary fibrosis by stimulating extracellular matrix (ECM) accumulation and activating fibroblasts. Here, we investigated the effects of Sal B on cell proliferation, collagen synthesis, endogenous TGF-β1 production, and α-smooth muscle actin (α-SMA, a marker of myofibroblasts) expression in human lung fibroblasts stimulated by TGF-β1 in vitro. ⋯ Interestingly, Sal B was found to inhibit TGF-β1-induced cell proliferation, expression of type I collagen, endogenous TGF-β1 production, and α-SMA expression in lung fibroblasts. Moreover, the inhibitory effect of Sal B on TGF-β1-induced proliferation and differentiation in lung fibroblasts was more significant when treated with high-dose Sal B (1 μmol/L versus 10 μmol/L, P < .05). These data demonstrate that Sal B inhibits TGF-β1-induced cell proliferation and differentiation in vitro experiment.