炎症体
氧化应激
炎症
TLR4型
机制(生物学)
MAPK/ERK通路
化学
吡喃结构域
细胞生物学
双酚A
信号转导
生物化学
免疫学
生物
有机化学
环氧树脂
哲学
认识论
作者
Chunfeng Xie,Miaomiao Ge,Jianliang Jin,Haie Xu,Li Mao,Shanshan Geng,Jieshu Wu,Jianyun Zhu,Xiaoting Li,Caiyun Zhong
标识
DOI:10.1016/j.jhazmat.2020.122549
摘要
Bisphenol S is considered as a safer alternative to bisphenol A. In the present study, we used murine macrophages to investigate the effects of BPS exposure on oxidative stress and inflammatory response as well as the underlying mechanism. Cells were exposed to BPS at various concentrations for short period of times. Results showed that 10-8 M BPS triggered oxidative stress by increasing ROS/RNS production, increased the levels of oxidant enzyme NOX1/2, and decreased the levels of antioxidant enzymes SOD1/2, CAT and GSH-Px. 10-8 M BPS exposure significantly induced the production of proinflammatory mediators. Activation of the NLRP3 inflammasome, TLR4, and MAPK pathways was involved in this process. Furthermore, we illustrated that NAC pretreatment diminished these effects triggered by BPS exposure. Collectively, our data suggested that BPS at a dose relevant to human serum concentration induced oxidative stress and inflammatory response in macrophages. These novel findings shed light on the concerns regarding the potential adverse effects of BPS exposure that requires further careful attention.
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