0000000000918724
AUTHOR
Federico Saibene
Carbocysteine reverses the effects of cigarette smoke and improves the effects of beclomethasone on the histone deacetylases in bronchial epithelial cells
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…
Carbocysteine counteracts the effects of cigarette smoke on cell growth and on the SIRT1/FoxO3 axis in bronchial epithelial cells
Abstract Background Cigarette smoke may accelerate cellular senescence by increasing oxidative stress. Altered proliferation and altered expression of anti-aging factors, including SIRT1 and FoxO3, characterise cellular senescence. The effects of carbocysteine on the SIRT1/FoxO3 axis and on downstream molecular mechanisms in human bronchial epithelial cells exposed to cigarette smoke are largely unknown. Aims Aim of this study was to explore whether carbocysteine modulated SIRT1/FoxO3 axis, and downstream molecular mechanisms associated to cellular senescence, in a bronchial epithelial cell line (16-HBE) exposed to cigarette smoke. Methods 16HBE cells were stimulated with/without cigarette …