The Inhibitory Effect Of Nap On Neurotoxicity Induced By Naf

Fluoride is commonly present in drinking water and toothpaste for preventing dental caries. However, it may induce neuronal damage as a potential neurotoxin. This study investigates the neuroprotective effects of NAP on NaF-induced apoptosis, establishing a research model to elucidate the relationship between oral fluoride exposure and systemic nervous system health;providind novel insights into the association between oral and nervous system disorders;offering a scientific basis on the use of fluorine-containing oral care products. A lentivirus vector overexpressing NAP was constructed and transfected into PC12 cells. The cells were divided into four groups: control, NAP-LV, NaF, and NaF +NAP-LV . After NaF treatment, the apoptosis rate was measured by Flow-cytometry;the expression levels of apoptosis-related proteins (Bax, Bcl-2, cleaved caspase-3, total caspase-3) ,microtubule end-binding proteins (EB1, EB2, EB3) in PC12 cells were analyzed using Western-blotting. Flow cytometry analysis revealed that NAP overexpression significantly suppressed the NaF-induced increase in apoptosis of PC12 cells. Western blot results demonstrated increased Bax expression and decreased Bcl-2 expression upon NAP overexpression in NaF-treated cells. Caspase-3 levels were markedly elevated, but no significant differences in cleaved caspase-3 were observed across groups. EB1 expression was substantially reduced in NaF-treated cells compared to other groups, while EB2 and EB3 levels showed no significant variation among all groups. NAP-LV is capable of inhibiting NaF-induced PC12 cell apoptosis through the upregulation of EB1 expression.