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Effect and its related mechanism of TNF-α on programmed necrosis of osteoblasts |
LIU Kai1 ZHUO Hongwu1 LIU Jianzhong2 KE Dianshan2▲ |
1.Department of Orthopedics, Fuzhou Second Hospital of Xiamen University, Fujian Province, Fuzhou 350007, China;
2.Department of Geriatrics Rehabilitation, Fujian Institute of Rehabilitation Industry Affiliated Rehabilitation Hospital of Fujian University of Traditional Chinese Medicine, Fujian Province, Fuzhou 350001, China |
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Abstract Objective To explore the effect and its related mechanism of TNF-α on programmed necrosis of osteoblasts. Methods Mice osteoblasts were isolated and cultured from suckling mice, and TNF-α was used to induce programmednecrosis of osteoblasts, Nec-1 was used to inhibit cell necrosis. Normal cultured osteoblasts were used as normal control group, and MTT assay was used to detect the cell proliferation. Tunel and Caspase 3 double staining was used to detect the programmed necrosis of osteoblasts. The expression of RIP1, RIP3 and MLKL were detected by Western blot. Results Compared with the normal control group, the proliferation activity of TNF-α group was decreased and the number of programmed necrosis was increased (P < 0.05). After the Nec-1 treatment, the proliferative activity was significantly increased compared with TNF-α group, and the number of programmed necrosis was decreased (P < 0.05). As time went on, the differences between the groups became more pronounced (P < 0.05). Compared with the normal control group, expression of RIP3 and MLKL protein in TNF-α group was significantly lower than that in normal control (P < 0.05). After the Nec-1 treatment, the expression of RIP3 and MLKL protein had significantly differences compared with TNF-α group (P < 0.05). Conclusion TNF-α can inhibit osteoblast proliferation and promote programmed necrosis of osteoblasts, which may be accomplished by reducing the expression of RIP3 and MLKL proteins in osteoblasts.
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