Fluorosis can induce neurotoxicity. Sodium butyrate (SB), a histone deacetylase inhibitor, has important research potential in correcting glucose metabolism disorders and is widely used in a variety of neurological diseases and metabolic diseases, but it is not yet known whether it plays a role in combating uoride-induced neurotoxicity. This study aims to evaluate the effect of SB on uoride neurotoxicity and the possible associated mechanisms. The results of HE staining and Morris water maze showed that in mice exposed to 100 mg/L uoride for three months, the hippocampal cells arranged in loosely with large cell gaps and diminished in number. In addition, 1000 mg/kg/day SB treatment improved uorideinduced neuronal cell damage and spatial learning memory impairment. Western blotting showed that the abundance of malate dehydrogenase 2 (MDH2) and pyruvate dehydrogenase (PDH) in the hippocampus of mice increased after uorosis, while the abundance of pyruvate kinase M (PKM), lactate dehydrogenase (LDH) and hexokinase (HK) decreased. SB treatment reversed the decreased glycolysis in the hippocampus of uorosis mice. We suspected that the PI3K/AKT/HIF-1α pathway may be involved in mediating the protective effects of SB against uorosis invasion in the hippocampus. These results suggested that SB could ameliorate uorosis-induced neurotoxicity, which might be linked with its function in regulating glycolysis as well as inhibition of the PI3K/AKT/HIF-1α pathway.
Fluorosis can induce neurotoxicity. Sodium butyrate (SB), a histone deacetylase inhibitor, has important research potential in correcting glucose metabolism disorders and is widely used in a variety of neurological diseases and metabolic diseases, but it is not yet known whether it plays a role in combating fluoride-induced neurotoxicity. This study aims to evaluate the effect of SB on fluoride neurotoxicity and the possible associated mechanisms. The results of HE staining and Morris water maze showed that in mice exposed to 100 mg/L fluoride for three months, the hippocampal cells arranged in loosely with large cell gaps and diminished in number. In addition, 1000 mg/kg/day SB treatment improved fluoride-induced neuronal cell damage and spatial learning memory impairment. Western blotting showed that the abundance of malate dehydrogenase 2 (MDH2) and pyruvate dehydrogenase (PDH) in the hippocampus of mice increased after fluorosis, while the abundance of pyruvate kinase M (PKM), lactate dehydrogenase (LDH) and hexokinase (HK) decreased. SB treatment reversed the decreased glycolysis in the hippocampus of fluorosis mice. We suspected that the PI3K/AKT/HIF-1α pathway may be involved in mediating the protective effects of SB against fluorosis invasion in the hippocampus. These results suggested that SB could ameliorate fluorosis-induced neurotoxicity, which might be linked with its function in regulating glycolysis as well as inhibition of the PI3K/AKT/HIF-1α pathway.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.