Mangiferin prevents the impairment of mitochondrial dynamics and an increase in oxidative stress caused by excessive fluoride in SH-SY5Y cells.
J Biochem Mol Toxicol
; 35(4): e22705, 2021 Apr.
Article
en En
| MEDLINE
| ID: mdl-33393728
ABSTRACT
Previous studies both invivo and in vitro have revealed that high levels of fluoride cause neurotoxicity. Mangiferin has been reported to possess antioxidant, antiapoptotic, and anti-inflammatory properties. The present study was designed to characterize the mechanisms by which mangiferin protects against NaF-induced neurotoxicity. Increased levels of proapoptotic Bax, Caspase-3, Caspase-9, and cleaved-caspase 3, as well as a decreased level of antiapoptotic Bcl-2 induced by fluoride in human neuroblastoma SH-SY5Y cells, these effects were prevented by pretreatment of mangiferin. In addition, mangiferin attenuated the enhancement of p-JNK, reductions of Nrf2 and HO-1, and increased level of the mitochondrial fission proteins Drp1 caused by fluoride. Moreover, oxidative stress, as reflected in the levels of reactive oxygen species, 8-hydroxy-2'-deoxyguanosine, and 4-hydroxynonenal, was elevated by fluoride and these effects were again ameliorated by mangiferin. In conclusion, protection by mangiferin against fluoride-induced neurotoxicity involves normalizing the impaired mitochondrial apoptotic pathway and dynamics and reducing oxidative stress via inactivation of the JNK and activation of the Nrf2/HO-1 pathways.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Estrés Oxidativo
/
Xantonas
/
Fluoruros
/
Mitocondrias
/
Proteínas de Neoplasias
/
Neuroblastoma
Límite:
Humans
Idioma:
En
Revista:
J Biochem Mol Toxicol
Asunto de la revista:
BIOLOGIA MOLECULAR
/
BIOQUIMICA
/
TOXICOLOGIA
Año:
2021
Tipo del documento:
Article
País de afiliación:
China