Isopsoralen ameliorates H2O2-induced damage in osteoblasts via activating the Wnt/β-catenin pathway.

Osteoporosis is a disease with a worldwide prevalence that involves a severe loss of bone mineral density and decreased microarchitecture, which increases the risk of bone fracture. The present study evaluated the effects of isopsoralen on osteoblastic OB-6 cells following hydrogen peroxide (H2O2)-induced damage and investigated the molecular mechanisms involved in this process. For in vitro experiments, OB-6 osteoblasts were treated with H2O2 or H2O2 + isopsoralen then the cell viability, apoptosis, reactive oxygen species (ROS) production and calcium accumulation were determined. Results demonstrated that treatment with H2O2 reduced cell viability, runt-related transcription factor 2 (RUNX2) and osteocalcin (OCN) expression levels, and calcium deposition, whilst markedly increasing cell apoptosis and ROS production. However, isopsoralen (1 µM) provided significant protection against H2O2-induced alterations in osteoblasts. In addition, isopsoralen effectively upregulated protein expression of tankyrase and β-catenin which are the main transductors of the Wnt/β-catenin pathway. Of note, the protective effects of isopsoralen against H2O2-induced damage were attenuated in OB-6 cells treated with tankyrase inhibitor XAV-939. In conclusion, the present findings provided evidence that isopsoralen attenuated oxidative stress-induced injury in osteoblasts via the Wnt/β-catenin signaling pathway.