The injury of fine particulate matter from cooking oil fumes on umbilical cord blood vessels in vitro
Lijuan Houa, Jian Zhanga, Chao Zhanga, Yachun Xua, Xiaoxia Zhua, Cijiang Yaoa, Ying Liua, Tao Lia, Jiyu Caob c✉
- aDepartment of Occupational and Environmental, School of Public Health, Anhui Medical University, Meishan Road, Hefei, Anhui, China
- bThe Teaching Center for Preventive Medicine, School of Public Health, Anhui Medical University, Meishan Road 81, Anhui Province, Postal Code 230032, Hefei, Anhui, China. Electronic address: qshq@163.com
- cThe Teaching Center for Preventive Medicine, School of Public Health, Anhui Medical University, Meishan Road 81, Anhui Province, Postal Code 230032, Hefei, Anhui, China
- ✉Corresponding author
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Abstract
Cooking oil fumes (COFs) derived PM 2.5 is the major source of indoor air pollution in Asia. For this, a pregnant rat model within different doses of cooking oil fumes (COFs) derived PM 2.5 was established in pregnancy in our research. Our previous studies have showed that exposure to COFs-derived PM 2.5 was related to adverse pregnancy outcomes. However, the mechanisms of signaling pathways remain unknown. Therefore, this study aimed to investigate the underlying mechanisms induced by COFs-derived PM2.5 injury on umbilical cord blood vessels (UCs) in vitro. Exposure to COFs-derived PM 2.5 resulted in changing the expression of eNOS, ET-1, ETRA, and ETRB. In additions, western blot analysis indicated that the HIF-1α/iNOS/NO signaling pathway and VEGF/VEGFR1/iNOS signaling pathway were involved in UCs injury triggered by COFs-derived PM 2.5 . In conclusion, our data suggested that exposure to COFs-derived PM 2.5 resulted in increasing of oxidative stress and inflammation, as well as dysfunction of UCs.
TL;DRExposure to COFs-derived PM2.5 resulted in increasing of oxidative stress and inflammation, as well as dysfunction of UCs, and western blot analysis indicated that the HIF-1α/iNOS/NO signaling pathway and VEGF/VEGFR1/ iNOS signaling pathway were involved in UCs injury triggered by COFs. (Semantic Scholar)