JNK and NADPH oxidase involved in fluoride-induced oxidative stress in BV-2 microglia cells.

摘要: Excessive fluoride may cause central nervous system (CNS) dysfunction, and oxidative stress is a recognized mode of action toxicity. In CNS, activated microglial cells can release more reactive oxygen species (ROS), NADPH oxidase (NOX) the major enzyme for production extracellular superoxide in microglia. ROS have been characterized as an important secondary messenger modulator various mammalian intracellular signaling pathways, including MAPK pathways. this study we examined TNF-α, IL-1β inflammatory cytokines releasing, expression MAPKs BV-2 microglia treated with fluoride. We found that increased JNK phosphorylation level pretreatment inhibitor SP600125 markedly reduced levels O2·− NO. NOX apocynin iNOS SMT dramatically decreased NaF-induced NO generations, respectively. Antioxidant melatonin (MEL) resulted reduction fluoride-stimulated The results confirmed played role inducing took part induced by meanwhile also could be fluoride-treated cells.