College of Veterinary Medicine, Northeast Agricultural University, Harbin, People's Republic of China.
College of Chemistry, Jilin University, Changchun, People's Republic of China.
Environ Toxicol. 2022 Oct;37(10):2552-2565. doi: 10.1002/tox.23618. Epub 2022 Jul 14.
Plastics are novel environmental pollutants with potential threats to the ecosystem. At least 5.25 trillion plastic particles in the environment, of which nanoplastics are <100 nm in diameter. Polystyrene nanoplastics (PS-NPs) exposure damaged the spleen's immune function. Lipopolysaccharide (LPS) induced other toxicants to damage cells and organs, triggering inflammation. However, the mechanism of PS-NPs aggravated LPS-induced spleen injury remains unclear. In this study, the PS-NPs or/and LPS mice exposure model was replicated by intraperitoneal injection of PS-NPs or/and LPS, and PS-NPs or/and LPS were exposed to RAW264.7 cells. The histopathological and ultrastructural changes of the mice spleen were observed by H&E staining and transmission electron microscope. Western Blot, qRT-PCR, and fluorescent probes staining were used to detect reactive oxygen species (ROS), oxidative stress indicators, inflammatory factors, and necroptosis-related indicators in mice spleen and RAW264.7 cells. The results showed that PS-NPs or LPS induced oxidative stress, activated the MAPK pathway, and eventually caused necroptosis and inflammation in mice spleen and RAW264.7 cells. Compared with the single treatment group, the changes in PS-NPs + LPS group were more obvious. Furthermore, ROS inhibitor N-Acetyl-L-cysteine (NAC) significantly inhibited the activation of the mitogen-activated protein kinase (MAPK) signaling pathway caused by co-treatment of PS-NPs and LPS, reducing necroptosis and inflammation. The results demonstrated that PS-NPs promoted LPS-induced spleen necroptosis and inflammation in mice through the ROS/MAPK pathway. This study increases the data on the damage of PS-NPs to the organism and expands the research ideas and clues.
塑料是新型环境污染物，对生态系统具有潜在威胁。环境中至少存在 5.25 万亿个塑料颗粒，其中纳米塑料的直径小于 100nm。聚苯乙烯纳米塑料（PS-NPs）暴露会损害脾脏的免疫功能。脂多糖（LPS）诱导其他有毒物质损害细胞和器官，引发炎症。然而，PS-NPs 加剧 LPS 诱导的脾脏损伤的机制尚不清楚。在本研究中，通过腹腔注射 PS-NPs 或/和 LPS 复制 PS-NPs 或/和 LPS 暴露的小鼠模型，并将 PS-NPs 或/和 LPS 暴露于 RAW264.7 细胞。通过 H&E 染色和透射电子显微镜观察小鼠脾脏的组织病理学和超微结构变化。Western Blot、qRT-PCR 和荧光探针染色用于检测小鼠脾脏和 RAW264.7 细胞中的活性氧（ROS）、氧化应激指标、炎症因子和坏死性凋亡相关指标。结果表明，PS-NPs 或 LPS 诱导氧化应激，激活 MAPK 通路，最终导致小鼠脾脏和 RAW264.7 细胞发生坏死性凋亡和炎症。与单一处理组相比，PS-NPs+LPS 组的变化更为明显。此外，ROS 抑制剂 N-乙酰-L-半胱氨酸（NAC）显著抑制 PS-NPs 和 LPS 共同处理引起的丝裂原活化蛋白激酶（MAPK）信号通路的激活，减少坏死性凋亡和炎症。结果表明，PS-NPs 通过 ROS/MAPK 通路促进 LPS 诱导的小鼠脾脏坏死性凋亡和炎症。本研究增加了 PS-NPs 对机体损伤的数据，并扩展了研究思路和线索。
