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Mitogen‐activated protein kinase signaling is involved in nonylphenol‐induced proinflammatory cytokines secretion by BV2 microglia
Author(s) -
Gu Weijia,
Wang Yi,
Qiu Zhenmin,
Dong Jing,
Wang Yuan,
Chen Jie
Publication year - 2018
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.3602
Subject(s) - proinflammatory cytokine , protein kinase a , protein kinase b , mapk/erk pathway , p38 mitogen activated protein kinases , microglia , activator (genetics) , neurotoxicity , signal transduction , ask1 , kinase , microbiology and biotechnology , inflammation , chemistry , biology , endocrinology , medicine , mitogen activated protein kinase kinase , immunology , biochemistry , toxicity , gene
Abstract Microglia (MG) are the key cells involved in the innate immune response in the central nervous system, and their activation has been linked to inflammation and neurotoxicity by the production of proinflammatory cytokines. Recently, researchers have found that nonylphenol (NP), a ubiquitous endocrine disrupting chemical, could impair neurodevelopment and cognitive memory performance. However, whether NP affects the inflammatory responses of MG remains to be elucidated. The aim of this study was to explore the effects of NP on the inflammatory responses of BV2 MG and the underlying mechanisms. Our results showed that NP increased the secretion of interleukin (IL)‐6 and IL‐1β in BV2 MG. Increased phosphorylation of Akt, JNK and p38 mitogen‐activated protein kinase and decreased phosphorylation of ERK were observed in NP‐treated MG. The inflammatory transcription factor activator protein 1 was also activated in NP‐treated BV2 MG. These results suggest that NP may activate Akt/mitogen‐activated protein kinase/activator protein 1 signaling in MG and subsequently increase IL‐6 and IL‐1β secretion.