lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells
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2018
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Abstract
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
| Reference Key |
ru2018internationallipopolysaccharide
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|---|---|
| Authors | ;Qin Ru;Qi Xiong;Lin Chen;Xiang Tian;Kai Yue;Baomiao Ma;Lu Liu;Rihui Wu;Congyue Xu;Mingshan Pi;Chaoying Li |
| Journal | management science letters |
| Year | 2018 |
| DOI |
10.13075/ijomeh.1896.00527
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| URL | |
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