Sodium Butyrate Alleviates Neuroinflammation in Fluorosis Mice by Suppressing NF-κB Signaling

Abstract

AbstractObjective:Excessive fluoride intake results in fluorosis, which is responsible for skeletal fluorosis and neuroinflammation. Fluoride activates microglia in the central nervous system to release inflammatory factors that exaggerate nerve injury. Sodium butyrate (NaB) has the potential to regulate the immune response; however, its function in fluorosis still needs to be clarified.Methods:This study involved the development of an animal model of chronic fluorosis, which was then treated with NaB.We evaluated animal activities, pathological features, and inflammation-associated signaling pathways in vivo and considered cell viability and inflammatory signaling in vitro.Results:The results revealed that NaB treatment induced a reliable preventative effect on fluorosis in mice based on restored learning and memory, decreased intranuclear NF-κB signaling, and inflammatory factors. Additionally, 0.2 mM NaB restored cell viability and corrected the elevated inflammatory signaling in BV-2 cells under sodium fluoride stress.Conclusion:NaB can alleviate fluorosis by suppressing NF-κB signaling and inflammasomes, providing a reliable method for the treatment of clinical fluorosis.