LAUSR

Previous studies have shown that the tumor necrosis factor-α (TNF-α) levels in serum and bone tissues form avascular necrosis of femoral head (ANFH) patients were higher than that of normal individuals, indicating TNF-α might play a role in the pathogenesis of ANFH. However, the underlying mechanisms remain unclear. Hematoxylin and Eosin (HE) staining was performed to show the pathological changes of ANFH bone tissues. TNF-α expression in normal and ANFH tissues was examined by qRT-PCR and western blot. Osteoblast autophagy and apoptosis, as well as signaling pathways activation, were measured by their corresponding marker proteins. Osteoblast proliferation, autophagy and apoptosis were evaluated using CCK-8, transmission electron microscope and flow cytometry. The structures of bone tissues of ANFH were obviously damaged. TNF-α expression was significantly upregulated in ANFH bone tissues compared to normal tissues. Autophagy and apoptosis were remarkably promoted, and p38 MAPK/NF-κB signaling pathways were markedly activated in ANFH. Suppression of p38 MAPK/NF-κB pathway significantly attenuated the TNF-α induced autophagy, however, enhanced the TNF-α induced apoptosis in osteoblast. Increased TNF-α in ANFH regulated osteoblast autophagy and apoptosis by p38 MAPK/NF-κB signaling pathways, blocking the pathway by inhibitors exacerbated TNF-α induced apoptosis through impairing the autophagy flux. This article is protected by copyright. All rights reserved.