- Qifeng Ren
- Wenfei Zhang
- Ping Li
- Jianli Zhou
- Zhonghao Li
- Yang Zhou
- Ming Li
Affiliations: Department of Joint Surgery, Dezhou People's Hospital, Dezhou, Shandong 253014, P.R. China, Department of Clinical Psychology, Dezhou People's Hospital, Dezhou, Shandong 253014, P.R. China, Department of Hematology, Dezhou People's Hospital, Dezhou, Shandong 253014, P.R. China, Department of Nuclear Medicine, Dezhou People's Hospital, Dezhou, Shandong 253014, P.R. China, Central Laboratory, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian 361004, P.R. China, Department of Joint Surgery, Dezhou People's Hospital, Dezhou, Shandong 253014, P.R. China
- Published online on: May 26, 2022 https://doi.org/10.3892/etm.2022.11397
Copyright: © Ren
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License [CC BY_NC 4.0].
Necrosis of the femoral head (NFH) is an orthopedic disease characterized by a severe lack of blood supply to the femoral head and a marked increase in intraosseous pressure. NFH is associated with numerous factors, such as alcohol consumption and hormone levels. The present study focused on the expression levels of osteoprotegerin (OPG) in NFH and the effect of OPG overexpression on chondrocyte apoptosis. The results demonstrated that OPG expression was markedly decreased in the femoral head of patients with NFH compared with normal femoral heads. Lentivirus‑mediated overexpression of OPG in human chondrocytes reversed the decrease in cell viability and the increase in reactive oxygen species production induced by an oxidative stress‑inducing factor, tert‑butyl hydroperoxide. Flow cytometry and TUNEL assays revealed that OPG overexpression inhibited the apoptosis of chondrocytes. In addition, it was revealed that OPG exerted its anti‑apoptotic effect mainly by promoting Bcl‑2 expression and Akt phosphorylation and inhibiting caspase‑3 cleavage and Bax expression. The present study revealed that OPG may be an important regulator of NFH.