气道重构是慢性哮喘的病理改变之一,涉及肺细胞外基质(ECM)沉积和降解失平衡.主要表现为ECM的沉积、基底膜增厚、气道平滑肌增生和肥厚等改变.

Objective To determine the effects of BRS-3 activation on apoptosis of bronchial epithelial cells.Methods Cell apoptosis was also measured with flow cytometer.Results Ozone exposure induced bronchial epithelial cell apoptosis,P3513 inhibited ozone exposure-induced cell apoptosis.Conclusion The date suggests that BRS-3 activation inhibites cell apoptosis.Therefore,a conclusion may be obtained that BRS-3 play an essential role in maintenance of integrity of bronchial epithelial cells in function during inflammation and exposure to a variety of inhaled and infectious agents,which has a possibility protective effect on asthma.

Objective To determine the effects of BRS-3 activation on MMPs release of human bronchial epithelial cells and MMP-9 and TIMP-1 on the proliferation of human lung fibroblasts.Methods Secretion of MMP-9 and TIMP-1 of human bronchial epithelial cells were assayed by ELISA; Proliferation of human lung fibroblasts was measured by MTT.Results Ozone exposure stimulated MMP-9、TIMP-1 release and decreased MMP-9/TIMP-1 ratio.P3513 inhibited ozone exposure-induced MMP-9、TIMP-1 release and made MMP-9/TIMP-1 ratio up.The effect of P3513 was diminished by PD98059,a inhibitor of mitogen activated protein kinase.MMP-9 stimulates proliferation of human lung fibroblasts,but TIMP-1 had no proliferation effect on this cells.Conclusion The date suggests that ozone exposure-induced MMP-9、TIMP-1 release and MMP-9/TIMP-1 can be regulated by BRS-3 activation dependent of mitogen activated protein kinase pathway in bronchial epithelial cell,and MMP-9 stimulates proliferation of human lung fibroblasts;Therefore,a conclusion may be obtained that BRS-3 play an essential role in airway remodeling,which has a possibility protective effect on asthma.