Effect of Nrf2/ARE Signaling Pathways on Oxidative Damage Induced by Sodium Fluoride in Rat Osteoblasts

To study the toxic mechanism of NaF on rat osteoblasts, the thiazole-blue tetrazole (MTT) method and alkaline phosphatase (ALP) method were used to evaluate the effect. Then, Comet assay was used to detect the effect of NaF on DNA damage in rat osteoblast model. NaF was selected to affect the rat osteoblast model at 1.00, 2.00, and 4.00 mmol/L concentration and measured the effect of sodium fluoride at different exposure concentrations of antioxidant enzyme activity and content of oxidative damage products (ROS), to further observe protein expressions of Nuclear Factor erythroid 2-Related Factor (Nrf2), Quinone oxidoreductase 1 (NQO1) and HO-1. We established the primary osteoblasts of suckling rats’ models by Sodium fluoride (NaF) to explore the oxidative stress and DNA damage of NaF in the rat osteoblasts. It was found that, the survival rate of rat osteoblasts decreased as the concentration of NaF was increased after exposal to NaF at certain concentrations, and the antioxidant function was impaired, leading to oxidative stress and DNA damage. Consequently, our results indicated that, the Nrf2/ARE signaling pathway was activated to initiate the expressions of downstream NQO1 and HO-1 antioxidant reactive proteins. In conclusion, the present study presented the oxidative stress of NaF in the rat osteoblasts at certain concentrations and DNA damage was observed. Nrf2 signaling was partly responsible for the oxidative stress induced by Sodium fluoride.