Authors: Jingying Zhu Lei Jiang Yanqing Liu Wenyi Qian Jingli Liu Jing Zhou Rong Gao Hang Xiao Jun Wang
Publish Date: 2014/07/22
Volume: 38, Issue: 2, Pages: 637-648
Abstract
Microglial activation has been reported to play an important role in neurodegenerative diseases by producing proinflammatory cytokines Bisphenol A BPA 22bis 4hydroxyphenyl propane known as a ubiquitous endocrinedisrupting chemical is reported to perform both mimic and antiestrogen properties however whether it affects cytokine production or immune response in central nervous system remains unclear The present study was aimed to explore whether BPA was involved in inflammatory action and to investigate the potential mechanisms in microglial cells BV2 the murine microglial cell line was used in the present work as the cell model BPAassociated morphologic changes cytokine responses and signaling events were examined using immunofluorescence analysis realtime PCR enzymelinked immunosorbent assay and western blot Our results indicated that BPA increased BV2 cells activation and simultaneously elevated tumor necrosis factorα and interleukin 6 expression which could be partially reversed by estrogen receptor antagonist ICI182780 In addition the cJun Nterminal protein kinase JNK inhibitor SP600125 rather than ERK1/2 blocker PD98059 displayed antiinflammatory properties on BPAelicited cytokine responses Moreover the inflammatory transcription factor NFκB was specifically activated by BPA as well These results taken together suggested that BPA may have functional effects on the response of microglial cell activation via in part the estrogen receptor JNK ERK mitogenactivated protein kinase and NFκB signaling pathways with its subsequent influence on proinflammatory action
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