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Our findings suggest that Clara cells inhibit pulmonary inflammation induced by crystalline silica via MMPs in vivo.
Natriuretic peptides inhibit pulmonary vascular smooth muscle proliferation and TGFβ-induced extracellular matrix expression in vitro, and prevent structural changes in vivo in animal models of PH (Jin et al., 1990; Klinger et al., 1998; 1999; Chen et al., 2006; Li et al., 2007).
On the other hand, platinum nanoparticles have anti-oxidant activity and inhibit pulmonary inflammation (e.g., as caused by exposure to cigarette smoke) [21 23].
Therefore, the ability of the combination to inhibit pulmonary metastasis was analyzed using metastatic animal models.
Hypercapnic acidosis appears to inhibit pulmonary epithelial wound healing by reducing cell migration via an NF-κB-dependent mechanism.
Heparin may inhibit pulmonary coagulation by affecting other cell types in the lung, including endothelial cells and fibroblasts.
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Nitroglycerin (as other vasodilators) may increase pulmonary shunt and aggravate systemic hypoxemia by inhibiting pulmonary hypoxic vasoconstriction.
These data suggest that Rg1 plays a protective role against LPS-induced ALI by ameliorating inflammatory responses, regulating the infiltration of M2 macrophages, and inhibiting pulmonary cell apoptosis.
Sesame oil may decrease pulmonary edema by inhibiting pulmonary inflammation in our animal model.
Furthermore, hypercapnia inhibits pulmonary epithelial wound repair also via an NF-κB mechanism [ 19].
The above findings suggest that IL-27 inhibits pulmonary fibrosis by regulating T lymphocyte differentiation in the spleen.
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