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首页> 外文期刊>Journal of toxicology and environmental health, Part A >Combined Effects of Fine Particulate Matter and Lipopolysaccharide on Apoptotic Responses in NR8383 Macrophages
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Combined Effects of Fine Particulate Matter and Lipopolysaccharide on Apoptotic Responses in NR8383 Macrophages

机译：细颗粒物和脂多糖对NR8383巨噬细胞凋亡反应的联合作用

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Alveolar macrophages (AM) are the predominant lung cells responsible for both ingestion and clearance of inhaled particulate matter (PM). The aims of this study were (1) to examine effects of fine PM on rat NR8383 cell line apoptosis, and (2) to determine whether NR8383 cell functions are further affected when exposed to fine PM in the presence of inflammation induced by lipopolysaccharide (LPS). Standard Reference Material 2786 (SRM 2786) for fine PM was used to measure the following parameters: cytotoxicity, apoptotic rate, Bax/Bcl-2 expression, nitric oxide (NO) production, and reactive oxygen species (ROS) generation in NR8383 cells. Data showed that SRM 2786 alone induced damage and apoptosis in NR8383 cells in a concentration-dependent manner as demonstrated by significant decrease in expression of Bcl-2 and increase in expression of Bax, suggesting fine PM might trigger apoptosis involving a mitochondria-mediated apoptotic pathway. In addition, there was elevated production of free radicals, such as NO and ROS, suggesting oxidative stress plays a role in the observed apoptotic responses. Further, LPS pretreatment enhanced apoptosis of NR8383 cells induced by SRM 2786. Consequently, data indicate that SRM 2786 triggered cell apoptosis in NR8383 cells, probably by mechanisms involving oxidative stress, as evidenced by elevated NO and ROS levels, while the degree of apoptosis was further aggravated by inflammation.
机译：肺泡巨噬细胞（AM）是主要的肺细胞，负责摄入和清除吸入颗粒物（PM）。这项研究的目的是（1）检查细微PM对大鼠NR8383细胞系凋亡的影响，以及（2）确定在脂多糖（LPS）诱导的炎症存在下，细微PM暴露于细微PM是否会进一步影响NR8383细胞功能）。用于精细PM的标准参考材料2786（SRM 2786）用于测量以下参数：NR8383细胞中的细胞毒性，凋亡率，Bax / Bcl-2表达，一氧化氮（NO）生成和活性氧（ROS）生成。数据显示，单独的SRM 2786可以以浓度依赖的方式诱导NR8383细胞的损伤和凋亡，这通过Bcl-2表达的显着减少和Bax表达的增加来证明，这表明细微PM可能触发涉及线粒体介导的凋亡途径的凋亡。此外，自由基（如NO和ROS）的产生增加，表明氧化应激在观察到的细胞凋亡反应中起作用。此外，LPS预处理增强了由SRM 2786诱导的NR8383细胞的凋亡。因此，数据表明SRM 2786可能通过涉及氧化应激的机制触发了NR8383细胞的细胞凋亡，如NO和ROS水平升高所证明的，而凋亡程度为炎症进一步加剧。

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