Epithelial injury cell-derived mediators

Cell-derived Mediators Implicated in Epithelial Injury... 

Bronchial Asthma. Figure 2 Mechanisms of bronchial hyperresponsiveness. Toxic products from eosinophils [cationic peptides, reactive oxygen species (ROS)] cause epithelial injury. Nerve endings become easily accessible to mediators from mast cells, eosinophils [eosinophil-derived neurotoxin (EDN)], and neutrophils, and to airborne toxicants such as S02. Activation of nerve endings stimulates effector cells like mucosal glands and airway smooth muscle either directly or by cholinergic reflexes. 

Caffeic Acid Phenethyl Ester (CAPE). CAPE, a phenolic compound with antioxidant properties, is an active ingredient derived from honeybee propolis (52). CAPE has antiviral, anti-inflammatory and antiproliferative properties. The compound differentially suppresses the growth of numerous human cancer cells and also inhibits tumor promoter-mediated processes in transformed cells (53,54). In transformed cells, CAPE induces apoptosis and inhibits the expression of the malignant phenotype (55,56). In addition, CAPE treatment attenuates the formation of azoxymethane-induced aberrant crypts and the activities of ornithine decarboxylase (ODC), tyrosin protein kinase, and lipoxygenase activity (57). Although the molecular basis for these multiple chemopreventive effects of CAPE is not clear, recent studies have demonstrated that CAPE is a potent and specific inhibitor of the transcription factor NF-kB (58). CAPE inhibited the activity and expression of COX-2 in the carrageenan air pouch model of inflammation as well as in TPA-treated human oral epithelial cells (59). CAPE was able to reduce neointimal formation by inhibiting NF-kB activation in a model of endothelial injury of rat carotid artery (60). 

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