| Objective To observe the damage of MSU (monosodium-urate) on osteoblasts and the mechanism and therapeutic effect of SFN (sulforaphane) on osteoblasts induced by MSU. Methods CCK-8 kit was used to detect osteoblast viability. Flow cytometry was used to detect the apoptosis. ROS levels were confirmed using ROS sensitive fluorescent probe. Drug concentration and duration of action were determined after MSU (10, 50, 100, 300, 500μg/mL) and SFN (1, 5, 10, 20, 50 μmol/L) were added respectively in osteoblasts culture medium for 0, 12, 24, 48, 72 h. Nrf2, HO-1, HIF-1, IL-6, and caspsae-3 in osteoblasts were detected using Western blotting. Results The toxic effect of MSU on osteoblasts activity increased along with the increase of concentration and time. Cell viability was less than 50% when the concentration was 300ug/ml and reaction time exceeded 48 hours. There was no effect on osteoblast viability when SFN was at 1 μmol/L and 10 μmol/L, but cell viability reduced when SFN was at 20 μmol/L and 50μmol/L. 300 μg/mL and 10 μmol/L were determined as action concentrations of MSU and SFN, respectively. 48 h was determined as action time. MSU increased the level of ROS in osteoblasts, while SFN decreased the ROS level and apoptosis rate in osteoblasts increased by MSU. SFN reduced the expression levels of HIF-1, IL-6, and caspase-3 in MSU induced osteoblasts, but increased the expression levels of Nrf2 and HO-1. Conclusion SFN reduces osteoblast damage induced by MSU. |