Vegf Receptor Inhibitors To Reduce Lung Inflammation In Mouse Asthma Model

Background: bronchial asthma is a chronic inflammatory disease of the airwayscharacterized by airway eosinophilia, goblet cell hyperplasia with mucus hypersecretion, andhyperresponsiveness, which usually induce increased vascular permeability, resulting inplasma exudation, is an endothelial cell-specific mitogenic peptide, which increases vascularpermeability and leads to airway inflammation. Vascular endothelial growth factor plays therole by binding to its receptors. The inhibition of Vascular endothelial growth factor receptormay be a good therapeutic strategy. SU5614, 5-Chloro-3-[(3,5-dimethylpyrrol-2-yl) methyl-lene]-2-indolinone, an inhibitor of vascular endothelial growth factor receptor tyrosinekinase has an ability of blocking vascular endothelial growth roles.Objective: An aim of the current paper was to study the effects SU5614, an VEGFreceptor inhibitor, on lung inflammation in OVA-induced asthma.Methods: A murine model for OVA-induced asthma was used in this study, the lunginflammation was assayed by H.E stain and VEGF level in lung was evaluated byimmunohistochemistry, VEGF level in cells of bronchoalveolar lavage fluid was measured byimmunocytochemistry.Results: The lung inflammation was significantly increased in asthma model groupcompare with control group. But the increased inflammation was decreased in SU5614 groupcompare with in asthma model group. VEGF level in lung and bronchoalveolar lavage fluidcells were more significantly increased in asthma model than in control group and weredecreased in SU5614 group compare with in asthma model group.Conclusion: These findings suggest that SU5614 may reduce lung inflammation throughdown-regulates VEGF level in a murine model of OVA-induced asthma.