Ru Qin, Xiong Qi, Chen Lin, Tian Xiang, Yue Kai, Ma Baomiao, Liu Lu, Wu Rihui, Xu Congyue, Pi Mingshan, Li Chaoying
Jianghan University, Wuhan, China (Wuhan Institutes of Biomedical Sciences).
Int J Occup Med Environ Health. 2018 Jan 7;31(2):173-183. doi: 10.13075/ijomeh.1896.00527. Epub 2017 Oct 11.
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.
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.
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).
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.
本研究旨在探讨细颗粒物标准参考物质（SRM 2786）对人肺支气管上皮细胞（16HBE细胞）细胞毒性和凋亡的影响。还确定了脂多糖（LPS）诱导的炎症是否会进一步加速SRM 2786刺激诱导的细胞凋亡。
将16HBE细胞暴露于不同剂量的SRM 2786，同时或不同时添加LPS。测量以下参数：细胞毒性、凋亡率、Bax/Bcl-2表达、一氧化氮（NO）产生和活性氧（ROS）生成。
结果表明，SRM 2786可诱导16HBE细胞损伤和凋亡，表现为Bcl-2表达显著降低和Bax表达增加。与对照细胞相比，用500μg/ml SRM 2786处理的细胞凋亡率从2.43±0.21%增加到43.96±2.95%（p<0.01）。此外，SRM 2786处理后NO和ROS的产生增加。用500μg/ml SRM 2786处理的细胞中NO水平为18.33±1.02μmol/l，而对照细胞为1.58±0.31μmol/l（p<0.01）。与对照组相比，用500μg/ml SRM 2786处理后细胞内ROS水平增加了24%（p<0.05）。此外，LPS预处理可能通过增加NO和ROS的产生，随后进行SRM 2786刺激来加速细胞凋亡。与仅用125μg/ml SRM 2786处理的细胞相比，用LPS预处理的细胞中NO和ROS水平分别增加了28%和11.6%（p<0.05），凋亡率从34.62±4.44%增加到54.11±3.34%（p<0.01）。
这些发现表明，体外暴露于SRM 2786可能通过涉及自由基产生的机制诱导16HBE细胞凋亡，而在炎症条件下凋亡程度会进一步加重。《国际职业医学与环境卫生杂志》2018年；31(2):173 - 183。
