Objective To investigate the potential roles of G protein-coupled receptor 30 (GPR30) in inhibiting apoptosis, oxidative stress response and inflammation in rat nucleus pulposus cells induced by interleukin-1β (IL-1β) via the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway.Methods Rat nucleus pulposus cells were treated with IL-1β to establish an in vitro model of intervertebral disc degeneration. The nucleus pulposus cells were divided into blank control (control) group, IL-1β group, IL-1β + GPR30 overexpression negative control plasmid (oe-NC) group, IL-1β + GPR30 overexpression plasmid (oe-GPR30) group, IL-1β + oe-GPR30 + Nrf2 interference negative control plasmid (si-NC) group and IL-1β + oe-GPR30 + Nrf2 interference plasmid (si-Nrf2) group, and the treatment concentration of IL-1β was 10 ng/ml. Quantitative real-time polymerase chain reaction was used to detect the mRNA expression of GPR30, and Western blotting was used to detect the protein expressions of GPR30, Nrf2, NAD(P)H dehydrogenase quinone 1 (NQO1) and heme oxygenase 1 (HO-1). The flow cytometry was performed to detect cell apoptosis. The levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured via enzyme-linked immunosorbent assay, while levels of reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured via corresponding commercial kits.Results Compared with the control group, the mRNA and protein expressions of GRP30 in nucleus pulposus cells were lower in the IL-1β group (P < 0.05). The mRNA and protein expressions of GRP30 in nucleus pulposus cells in the IL-1β + oe-GPR30 group were higher than those in the IL-1β + oe-NC group (P < 0.05). The relative protein expression of Nrf2 in the nucleus of nucleus pulposus cells in the IL-1β group was higher than that in the control group (P < 0.05), while that in the IL-1β + oe-GPR30 group was higher than that in the IL-1β + oe-NC group (P < 0.05). The relative protein expressions of Nrf2, HO-1 and NQO1 in nucleus pulposus cells in the IL-1β group were lower than those in the control group (P < 0.05), and those in the IL-1β + oe-GPR30 group were higher than those in the IL-1β + oe-NC group (P < 0.05). The relative protein expression of Nrf2 in nucleus pulposus cells in the IL-1β group was lower (P < 0.05), that in the IL-1β + oe-GPR30 group was higher than that in the IL-1β + oe-NC group (P < 0.05), and that in the IL-1β + oe-GPR30 + si-Nrf2 group was lower than that in the IL-1β + oe-GPR30 + si-NC group (P < 0.05). The apoptosis rate of nucleus pulposus cells in the IL-1β group was higher than that in the control group (P < 0.05), that in the IL-1β + oe-GPR30 group was lower than that in the IL-1β + oe-NC group (P < 0.05), and that in the IL-1β + oe-GPR30 + si-Nrf2 group was higher than that in the IL-1β + oe-GPR30 + si-NC group (P < 0.05). The levels of TNF-α and IL-6 in the IL-1β group were higher than those in the control group (P < 0.05), those in the IL-1β + oe-GPR30 group were lower than those in the IL-1β+oe-NC group (P < 0.05), and those in the IL-1β + oe-GPR30 + si-Nrf2 group were higher than those in the IL-1β + oe-GPR30 + si-NC group (P < 0.05). Compared with the control group, the levels of ROS and MDA were higher and the level of SOD was lower in the IL-1β group (P < 0.05). Compared with the IL-1β + oe-NC group, the levels of ROS and MDA were lower and the level of SOD was higher in the IL-1β + oe-GPR30 group (P < 0.05). Compared with the IL-1β + oe-GPR30+si-NC group, the levels of ROS and MDA were higher and the level of SOD was lower in the IL-1β + oe-GPR30 + si-Nrf2 group (P < 0.05).Conclusions Up-regulation of the expression of GPR30 activates the Nrf2/ARE signaling pathway and inhibits IL-1β-induced apoptosis, inflammation and oxidative stress in nucleus pulposus cells.