ABSTRACT
BACKGROUND: Tumor necrosis factor α (TNF-α) is a pro-inflammatory factor that can induce osteoblast apoptosis and enhance osteoclast function, resulting in inflammatory bone destruction. However, the specific mechanism is unclear. OBJECTIVE: To investigate the effect of TNF-α on the proliferation and apoptosis of MLO-Y4 cells and the possible mechanism. METHODS: MLO-Y4 cells were divided into control group, TNF-α group and ERK1/2 inhibitor group, followed by incubation with α-MEM complete medium containing nothing, 50 μg/L TNF-α, and 50 μmol/L PD98059 for 24 hours, respectively. Cell proliferation was detected by MTT method, and cell apoptosis were detected by flow cytometry. To assess the level of oxidative stress, malondialdehyde, superoxide dismutase, and glutathione peroxidase levels were detected. The protein levels of PCNA, cleaved Caspase-3, p-ERK1/2 and ERK1/2 were measured by western blot. RESULTS AND CONCLUSION: Compared with the control group, treatment with 50 μg/L TNF-α for 24 hours reduced the cell proliferation ability and increased the apoptosis rate increased; levels of lipid peroxidase and malondialdehyde increased significantly, whereas the activities of superoxide dismutase and glutathione peroxidase decreased significantly. Compared with the control group, significantly decreased PCNA and p-ERK1/2 as well as significantly up-regulated cleaved caspase-3 were observed in the TNF-α group; however, the expression of total protein ERK1/2 remained unchanged. There was no significant difference between the ERK1/2 inhibitor group and TNF-α group. To conclude, 50 μg/L TNF-α can decrease the proliferation and increase the apoptosis of MLO-Y4 cells. The mechanism may be related to the inhibition of ERK1/2 signaling pathway.