Bisphenol A disrupts inflammatory responses via Nod-like receptor protein 3 pathway in macrophages

Bisphenol A (BPA) is a harmful endocrine disruptor that is found in polycarbonate plastics such as plastic food containers and in epoxy resins such as dental resins. In the current study, we investigated the effect of BPA on function of inflammatory responses involving activation of Nod-like receptor protein 3 (NLRP3) inflammasome. Treatment with BPA decreased nitric oxide (NO) production and expression levels of inducible NO synthase (iNOS), prostaglandin E-2 (PGE(2)), and cyclooxygenase (Cox)-2 in RAW 264.7 macrophages. BPA also suppressed activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B activity (NF-kappa B). BPA significantly down-regulated the secretion of pro-inflammatory cytokines including tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-1 beta, and IL-18. The decreased production of IL-1 beta and IL-18 induced by BPA was associated with inactivation of the activity of the NLRP3 inflammasome. Collectively, these data suggested that BPA could act as a disruptor of the inflammation activity by regulating the NF-kappa B/MAPK pathways and NLRP3 inflammasome activation.