Objective To investigate the effects of bortezomib ( Bor) on nuclear factor _κB ( NF-_κB) and inflammatory damage in ATDC5 cells induced by interleukin-1β (IL-1β). Methods ATDC5 cells were treated with (0, 5, 15, 25, 35, 45, 55) nmol/L Bor for 48 hours, and CCK-8 was used to determine the cytotoxic concentration of Bor. ATDC5 cells were co-cultured for 48 hours with (0, 1. 0, 5. 0, 12. 5, 25. 0) nmol/L Bor and 10 μg/mL IL-1β. CCK-8 was used to detect cell proliferation and apoptosis was detected by flow cytometry. IL-1β in supernatant was detected using an enzyme-linked immunosorbent assay (ELISA), and the levels of NF-_κB, B-cell lymphoma/leukemia-2 proto oncogene (BcL2) and BcL2-related X protein (BAX) were determined by Western blot. Results There was no significant difference in (0, 5, 15, 25) nmol/L Bor group (P >0. 05). Compared with the 0 nmol/L Bor group, the cell survival rate of the 35, 45, and 55 nmol/L Bor groups was reduced (P <0. 05). A concentration of ≤25 nmol/L Bor was non-toxic to the cells. Compared with the 0 nmol/L Bor group, the cell survival rate and BcL2 protein level in the IL-1β group was decreased (P <0. 05), and the apoptosis rate, IL-1β level in the supernatant, and NF-_κB and BAX protein levels were increased (P <0. 05). With increasing Bor dose, the cell survival rate and the level of BcL2 protein in cells gradually increased (P <0. 05), while the apoptosis rate, the level of IL-1β in supernatant, and the levels of NF-_κB and BAX proteins in cells gradually decreased (P <0. 05) in a dose-dependent manner. Conclusions Bor can inhibit apoptosis and reduce the levels of inflammatory factors, thereby reducing inflammatory damage to ATDC5 cells induced by IL-1β, which may occur via inhibition of the NF-_κB pathway.