Hyperoside decreases the apoptosis and autophagy rates of osteoblast MC3T3-E1 cells by regulating TNF-like weak inducer of apoptosis and the p38mitogen activated protein kinase pathway

Wear particles generated between the interface of joints and artificial joint replacements are one of the primary causes of aseptic loosening. The aim of the present study was to investigate the influence of titanium (Ti) particles on the apoptosis and autophagy of osteoblasts, and probe into the potential use of hyperoside (Hy) as a protector for osteoblasts in Ti particle-induced injury. MC3T3-E1 cells were divided into control, Ti, Hy-1+Ti and Hy-2+Ti groups. Cell viability was detected using a Cell Counting Kit-8 assay. Apoptosis and autophagy rates were determined using flow cytometry. Expression levels of apoptosis-associated genes, including caspase-3, apoptosis regulator BAX, apoptosis regulator Bcl-2 and cellular tumor antigen p53, in addition to autophagy-associated genes, including Beclin1 and microtubule-associated protein light chain 3 conversion LC3-II/I, were measured using reverse transcription-quantitative polymerase chain reaction and western blotting. Activation of the tumor necrosis factor ligand superfamily member 12 (TWEAK)-mitogen activated protein kinase 11 (p38) mitogen activated protein kinase (MAPK) pathway was observed by western blotting. The present study demonstrated that pretreatment with Hy was able to increase cell viability and proliferation, and decrease apoptosis and autophagy to protect MC3T3-E1 cells against Ti particle-induced damage. Activation of the TWEAK-p38 pathway contributed to the repair processes of treatment with Hy. The present results suggested that Hy protected osteoblasts against Ti particle-induced damage by regulating the TWEAK-p38 pathway, which suggested the potential of Hy as a protective agent for bones.