Lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells

• Authors: Qin Ru , Qi Xiong , Lin Chen , Xiang Tian , Kai Yue , Baomiao Ma , Lu Liu , Rihui Wu , Congyue Xu , Mingshan Pi , Chaoying Li

Abstracts

EN

Objectives The aim of the study has been to investigate the effect of the Standard Reference Material of fine particulate matter (SRM 2786) on cytotoxicity and apoptosis in human lung bronchial epithelial cells (16HBE cells). Whether the lipopolysaccharide (LPS)-induced inflammation could further accelerate cell apoptosis induced by SRM 2786 stimulation has also been determined. Material and Methods 16HBE cells were exposed to various doses of SRM 2786 with or without LPS. The following parameters: cytotoxicity, apoptotic rate, Bax/Bcl-2 expression, nitric oxide (NO) production, and reactive oxygen species (ROS) generation were measured. Results The results have shown that SRM 2786 induces cell damage and apoptosis of 16HBE cells as demonstrated by significant decrease in expression of Bcl-2 and increase in expression of Bax. When compared with the control cells, the apoptotic rate of cells treated by 500 μg/ml of SRM 2786 increased from 2.43±0.21% to 43.96±2.95% (p < 0.01). Further, there was an elevated production of NO and ROS post SRM 2786 treatment. The level of NO in cells treated with 500 μg/ml of SRM 2786 was 18.33±1.02 μmol/l whereas that of control cells was 1.58±0.31 μmol/l (p < 0.01). When compared with the control group, the level of intracellular ROS increased by 24% after treatment with 500 μg/ml of SRM 2786 (p < 0.05). In addition, LPS pre-treatment may accelerate cell apoptosis by increasing generation of NO and ROS followed by SRM 2786 stimulation. When compared to cells treated with 125 μg/ml of SRM 2786 alone, the levels of NO and ROS in cells pretreated with LPS increased by 28% and 11.6%, respectively (p < 0.05), and the apoptotic rate increased from 34.62±4.44% to 54.11±3.34% (p < 0.01). Conclusions These findings have suggested that in vitro exposure to SRM 2786 could induce 16HBE cells apoptosis probably by means of the mechanism involving the generation of free radicals, while the degree of apoptosis would be further aggravated under inflammation condition. Int J Occup Med Environ Health 2018;31(2):173–183

Keywords

EN

Apoptosis; cytotoxicity; inflammation; fine particulate matter; free radicals; bronchial epithelial cells

• Publisher: Instytut Medycyny Pracy im. prof. dra Jerzego Nofera w Łodzi
• Journal: International Journal of Occupational Medicine and Environmental Health
• Year: 2017
• Volume: 31
• Issue: 2
• Pages: 173-183

Dates

published

2018

Contributors

author

Qin Ru

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

author

Qi Xiong

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

author

Lin Chen

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

author

Xiang Tian

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

author

Kai Yue

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

author

Baomiao Ma

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

author

Lu Liu

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

author

Rihui Wu

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

author

Congyue Xu

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

author

Mingshan Pi

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)

author

Chaoying Li

• Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences)
• Hanjea Biological Technology (Wuhan) Co., Ltd., Wuhan, China (Hanjea Institutes of Biomedical Sciences)

Identifiers

DOI

10.13075/ijomeh.1896.00527

Biblioteka Nauki

2161782