Oxidative stress plays an important role in the pathophysiology of emphysema through activation of proteases and tissue apoptosis. We have studied the effects of ozone, exposing BALB / C mice or one 3-hour exposure or multiple impact on
3 or 6 weeks, with two 3-s exposures per week. Compared to air exposed mice, the increase in neutrophils in bronchoalveolar
washing liquid and pneumonia rate was highest in mice at 3 and 6 weeks. Lung volumes were increased in the third
6 weeks, the exposed mice, but not one that affected. Alveolar space and the mean linear intercept were increased in 6 - and not three weeks, exposed mice.
Caspase-3 and apoptosis protease activating factor-1 imunoreaktyvnosti was increased in the airways and alveolar epithelium lasix heart and macrophages
3rd, 6-week exposed mice. IL-13, keratinocyte hemoattraktantnyy, caspase-3 and IFN-γ mRNA
increased in 6-week-group that has influence, but hemoksihenazy-1 (HO-1) mRNA decreased. matrix metalloproteinazy-12 (MMP-12) and
caspase-3 protein expression is increased in the lungs 6 weeks, exposed mice. Collagen area increased and decreased epithelial area
in the airway wall in the third 6-week exposure. Effect of ozone mice for 6 weeks caused a chronic inflammatory process of alveolar
extension and damage associated with epithelial apoptosis and increased expression of proteases. . << >>
No comments:
Post a Comment