Carbocysteine reverts the effects of cigarette smoke on the growth and on the senescence of bronchial epithelial cells

Cigarette smoke exposure, increasing oxidative stress, may accelerate senescence processes. The effects of carbocysteine on the molecular mechanisms of cellular senescence in human bronchial epithelial cells stimulated with cigarette smoke extracts (CSE) are largely unknown. This study was aimed to explore whether carbocysteine, in a bronchial epithelial cell line (16-HBE), counteracted some CSE-mediated effects and in particular some molecular mechanisms associated to cellular senescence. Methods: Bronchial epithelial cells were stimulated with CSE and/or carbocysteine. Cell proliferation was assessed by flow-citometry (72 hours colture) and by clonogenic assay (21 days colture); SIRT-1 and FOXO-3 expression were assessed by flow-citometry and by western blot analysis, respectively. Results: CSE decreased cell proliferation as well as the expression of SIRT-1 and FOXO-3. Carbocysteine in CSE stimulated bronchial epithelial cells reverted these phenomena increasing the cell proliferation, the expression of SIRT-1 and of FOXO-3. In conclusion, the present study provides compelling evidences that carbocysteine may contribute to revert some senescence processes induced by oxidative stress due to cigarette smoke exposure.