Nicotine Induces Apoptosis of BEAS-2B Cells by Inhibiting Autophagy via the PI3K / Akt / mTOR Pathway / 中国生物化学与分子生物学报

ABSTRACT

Cigarette smoking is a major risk factor for chronic respiratory inflammatory diseases. Nicotine is the most important ingredient in tobacco smoke. The incidence rate of chronic respiratory diseases associated with nicotine is increasing rapidly. Therefore, it is urgent to find potential targets for nicotine-related chronic respiratory inflammatory diseases. This article hereby aims to investigate the effect of nicotine on apoptosis of BEAS-2B cells and its potential mechanism. The expressions of apoptosis, autophagy and PI3K/ Akt/ mTOR pathway-related proteins were detected by Western blotting. Flow cytometry and CCK-8 were used to detect cell apoptosis rate and cell viability. The results showed that nicotine induced apoptosis of BEAS-2B cells at 1, 2 and 4 mmol/ L, and the cell viability decreased with the increase of concentration. Compared with the control group, the expression of autophagy-related protein LC3Ⅱ and P62 increased significantly after nicotine treatment (P0. 05). Compared with the nicotine group, rapamycin pretreatment significantly decreased cell apoptosis and increased cell activity (P<0. 05). Compared with the nicotine group, the expression of p-Akt and p-mTOR decreased significantly and apoptosis decreased significantly after LY294002 pretreatment (P<0. 05). Furthermore, nicotine induces apoptosis of BEAS-2B cells by inhibiting autophagy may be via PI3K/ Akt/ mTOR pathway, which may be a potential target for the prevention and treatment of chronic respiratory inflammatory diseases.