[Protection from oxidant injury on airway epithelial cells and the local microenvironment modulation]

An cellular injury model of primary cultured rabbit bronchial epithelial cells (BEC) exposed to ozone was established in this study and cytoprotective effects of factors in local microenvironment of airway such as vasoactive intestinal peptide (VIP), epidermal growth factor (EGF) and heat stress were observed. These factors could lighten damage in cell and elevate the level of glutashione(GSH), which depended upon phosphorylation modulation by protein kinases and gene transcription. A low level of bcl-2 gene expression could be detected in BEC at basic state, and either VIP or EGF stimulated the transcription of bcl-2, which improved the capability of BEC to resist oxidant injury. Otherwise, EGF and heat stress increased VIP autocrine from BEC and upregulated the expression of VIP receptor on BEC, so that the protective effect of VIP can be amplified in local sites. This study confirmed that there is an anti-injury protection on airway epithelium and the protection can be adaptively modulated by the regulatory peptides in local microenvironment and exogenous stimulus.