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Published on: June 9, 2017
Chronic Arsenic Exposure Induces Neuroinflammation by Regulating the Nrf2/NLRP3 Inflammasome Signaling Pathway
Jianyu Qu1,2, Changyi Pi1, Ying Ma1
1Hunan Engineering Research Center of Livestock and Poultry Health Care, College of Veterinary Medicine, Hunan Agricultural University, Changsha, Hunan Province 410128, China.
Abstract:
Arsenic, an environmental toxic metalloid, readily crosses the blood-brain barrier to induce neurotoxicity, but the mechanism of chronic arsenic exposure-induced brain damage remains unclear. In this study, results demonstrated that chronic NaAsO2 exposure damaged hippocampal neurons, increased the production of pro-inflammatory cytokines, and caused oxidative stress in mice and SH-SY5Y cells. Besides, chronic NaAsO2 exposure decreased the levels of the Nrf2 signaling pathway-related mRNA/protein while increasing the levels of the NLRP3 inflammasome-related mRNA/protein. CBR-470-1 (a Nrf2 activator) pretreatment mitigated NaAsO2 exposure-induced oxidative stress and neuroinflammation by regulating the Nrf2/NLRP3 inflammasome signaling pathway in SH-SY5Y cells. Meanwhile, MCC950 (a NLRP3 inhibitor) pretreatment alleviated NaAsO2-induced neuroinflammation by inhibiting the NLRP3 inflammasome activation without affecting the Nrf2 signaling pathway in SH-SY5Y cells. In conclusion, chronic NaAsO2 exposure induced oxidative stress and neuroinflammation in mice and SH-SY5Y cells through regulation of the Nrf2/NLRP3 inflammasome signaling pathway, which provides a theoretical basis for preventing chronic arsenic exposure-induced neurotoxicity.
