期刊
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
卷 188, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2019.109905
关键词
COFs-derived PM2.5/VD3/HUVECs/NLRP3/Tube formation
资金
- National Natural Science Foundation of China [81872580]
- Natural Science Foundation of Anhui Province [1708085MH220]
- Anhui Province Science and Technology Innovation Project Demonstration Project [201707d08050003]
- Foundation of Natural Science for Colleges and Universities in Anhui Province [KJ2018A0167]
- Project Foundation for the Young Talents in Colleges of Anhui Province [gxyq2017003]
- Grant for Scientific Research of BSKY from Anhui Medical University [XJ201621]
- Student's Platform for Innovation and Entrepreneurship Training Program of China [201810366031]
Cooking oil fumes-derived PM2.5 (COFs-derived PM2.5) is the main source of indoor pollution. Exposure to COFs-derived PM2.5 can cause oxidative stress and affect angiogenesis. Here we investigated the roles of vitamin D-3 (VD3) in protecting tubule formation injury induced by COFs-derived PM2.5, and the roles of ROS/NLRP3/VEGF signaling pathway in the effects. Human umbilical vein endothelial cells (HUVECs) were exposed to 0 (1 parts per thousand DMSO), 1000 nmol/l VD3, 100 mu g/ml PM2.5, and 1000 nmol/l VD3 + 100 mu g/ml PM2.5, respectively. Cell viability and tube formation, as well as protein and mRNA levels were measured. The results showed that exposure of COFs-derived PM2.5 dose-and time-dependently reduced the viability of HUVECs, increased the levels of mitochondrial and intracellular ROS, and changed the mitochondrial membrane potential level. While co-incubation with VD3 rescued these adverse effects. Both Western blot and real-time PCR (RT-PCR) showed that the expressions of NLRP3, caspase-1, Interleukin (IL)-1 beta, and IL-18 in COFs-derived PM2.5 exposure group increased significantly, which could be effectively decreased by co-incubation with VD3. COFs-derived PM2.5 exposure could also reduce the expression of VEGF, while co-incubating HUVECs with VD3 evidently up-regulated the protein level of VEGF in HUVECs. In addition, COFs-derived PM2.5 could also inhibit the tube formation of HUVECs in vitro, which could be effectively rescued by the co-incubation of VD3. Our study proved that COFs-derived PM2.5 could damage the tubule formation of HUVECs in vitro, which could be effectively rescue by co-incubation with VD3, in which processes the ROS/NLRP3/VEGF signaling pathway played a crucial role. It provides a new theoretical basis for further study on the toxicity of PM2.5 to umbilical cord blood vessels.
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