| Objective To investigate the effect of picroside II on dexamethasone (DEX)-induced osteoblast apoptosis by regulating the receptor-interacting protein (RIP) 1/RIP3/mixed lineage kinase domain-like (MLKL) signal. Methods HFOB 1.19 cells were cultured in vitro and randomly grouped into control group, DEX group, DEX+picroside II group, DEX+RIP1 overexpression group, DEX+empty plasmid group, and DEX+picroside II+RIP1 overexpression group. After grouping treatment, cell viability rate, apoptosis rate, the relative level of reactive oxygen species (ROS), the releases of lactate dehydrogenase (LDH), interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, the relative expressions of BCL-2 and BAX, the expressions of RIP1/RIP3/MLKL signal proteins were detected in cells of each group. Results Compared to those in the control group, the cell viability and the relative expression of BCL-2 in DEX group decreased (P<0.05), the apoptosis rate, ROS relative level, LDH and IL-1β, TNF-α, IL-6 releases, and the relative expressions of BAX and RIP1, RIP3, MLKL proteins increased (P<0.05). Compared to those in DEX group, the cell viability and the relative expression of BCL-2 in DEX+picroside II group increased (P<0.05), the apoptosis rate, ROS relative level, LDH and IL-1β, TNF-α, IL-6 releases, and the relative expressions of BAX and RIP1, RIP3, MLKL proteins decreased (P<0.05). The cell viability and the relative expression of BCL-2 in the DEX+RIP1 overexpression group decreased (P<0.05), the apoptosis rate, ROS relative level, LDH and IL-1β, TNF-α, IL-6 releases, and the relative expressions of BAX and RIP1, RIP3, MLKL proteins increased (P<0.05). There was no obvious difference in cell indexes in DEX+empty plasmid group (P>0.05). Overexpression of RIP1 weakened the effect of picroside II on DEX induced hFOB 1.19 cells. Conclusion Picroside II reduces inflammation by down-regulating RIP1/RIP3/MLKL pathway, thus inhibiting the apoptosis of osteoblasts induced by DEX. |