6533b851fe1ef96bd12aa048

RESEARCH PRODUCT

Carbocysteine reverses the effects of cigarette smoke and improves the effects of beclomethasone on the histone deacetylases in bronchial epithelial cells

subject

description

Cigarette smoke exposure, increasing oxidative stress, may negatively affect histone deacetylase expression/activity. Histone deacetylase expression/activity and in particular HDAC2, HDAC3, and SIRT-1 may control inflammation, cell senescence and responses to corticosteroids. The effects of carbocysteine and of beclomethasone on the histone deacetylase expression/activity in human bronchial epithelial cells stimulated with cigarette smoke extracts (CSE) are largely unknown. This study was aimed to explore whether carbocysteine and beclomethasone, in a bronchial epithelial cell line (16-HBE) exposed to CSE, were able to modulate the expression/activity of HDAC2, HDAC3, and of SIRT-1. Methods: Bronchial epithelial cells were stimulated with CSE and/or carbocysteine, and/or beclomethasone. Nuclear extracts were analysed by western blot analysis and by a colorimetric enzymatic assay , for histone deacetylase expression and activity, respectively. Results: CSE decreased the nuclear expression as well as the activity of histone deacetylases. Carbocysteine in CSE stimulated bronchial epithelial cells reverted these phenomena and further increased the effects of beclomethasone increasing the expression and the activity of histone deacetylases. In conclusion, the present study provides compelling evidences that carbocysteine may restore histone deacetylase expression/activity as well as may improve corticosteroids responses in bronchial epithelial cells exposed to cigarette smoke. Funded by Consiglio Nazionale delle Ricerche and by Dompe.