Author: Xie, Xin-Hui; Wang, Xin-Luan; Yang, Hui-Lin; Zhao, De-Wei; Qin, Ling
Title: Steroid-associated osteonecrosis: Epidemiology, pathophysiology, animal model, prevention, and potential treatments (an overview) Document date: 2015_1_13
ID: y6y235hw_32
Snippet: Oxidation injury was another pathogenesis for SAON. It was reported that oxidative injury in BMSCs was demonstrated shortly (3 days) after the administration of MPSL in a rabbit model prior to ON development [30] . The significant increased rate of ON development by using antioxidant showed that the oxidation injury was not only involved in the early stage of SAON [27] . Tissue oxidation was proven to be able to induce cells apoptosis through oxy.....
Document: Oxidation injury was another pathogenesis for SAON. It was reported that oxidative injury in BMSCs was demonstrated shortly (3 days) after the administration of MPSL in a rabbit model prior to ON development [30] . The significant increased rate of ON development by using antioxidant showed that the oxidation injury was not only involved in the early stage of SAON [27] . Tissue oxidation was proven to be able to induce cells apoptosis through oxygen free radicals. Oxidative stress inhibited osteogenic differentiation of primary rabbit BMSCs and calvarial osteoblasts by stimulating extracellular signal-regulated kinases (ERKs) and nuclear factor-kB [31] , implying decreased bone formation in SAON.
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