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Cigarette smoke (CS) is one of the severe risk factors for the development of the pulmonary disease. However, the underlying mechanisms, especially the CS-induced the human bronchial epithelial cells (BEAS-2B) apoptosis related to endoplasmic reticulum stress (ERS) and autophagy, remains to be studied. This study aims to investigate the relationship between ERS and autophagy in apoptosis induced by CS condensate (CSC). BEAS-2B cells were stimulated with 0.02, 0.04 and 0.08 mg/ml CSC for 24 h to detect the ERS, autophagy and apoptosis. Then, ERS and autophagy of BEAS-2B cells were inhibited, respectively, by using 4-PBA and 3-MA, and followed by CSC treatment. The results showed that CSC decreased cell viability, increased cell apoptosis, elevated cleaved-caspase 3/pro-caspase 3 ratio and Bax expressions, but decreased Bcl-2 expressions. The GRP78 and CHOP expressions and LC3-II/LC3-I ratio were dose-dependently increased. The structure of the endoplasmic reticulum was abnormal and the number of autolysosomes was increased in BEAS-2B cells after CSC stimulation. The LC3-II/LC3-I ratio was decreased after ERS inhibition with 4-PBA, but GRP78 and CHOP expressions were enhanced after autophagy inhibition with 3-MA. CSC-induced apoptosis was further increased, Bax expressions and cleaved-caspase 3/pro-caspase 3 ratio were improved, but Bcl-2 expressions were decreased after 3-MA or 4-PBA treatment. In conclusion, the study indicates that ERS may repress apoptosis of BEAS-2B cells induced by CSC via activating autophagy, but autophagy relieves ERS in a negative feedback. This study provides better understanding and experimental support on the underlying mechanisms of pulmonary disease stimulated by CS.

The relationship between endoplasmic reticulum stress and autophagy in apoptosis of BEAS-2B cells induced by cigarette smoke condensate