Geniposide attenuates cadmium‑induced oxidative stress injury via Nrf2 signaling in osteoblasts.

Geniposide, as a type of iridoid glycoside, has antioxidative capacity. However, the mechanism underlying the effect of geniposide in cadmium (Cd)‑induced osteoblast injury remains only partly elucidated. In the present study, Cell Counting Kit‑8 (CCK‑8) was used to determine MC‑3T3‑E1 cell viability. Flow cytometry was used to determine the rate of apoptosis and levels of reactive oxygen species (ROS). Oxidative stress‑related factors were assessed using enzyme‑linked immunosorbent method (ELISA). Quantitative real‑time polymerase chain reaction (qPCR) and western blotting were used to evaluate apoptosis‑ and bone formation‑related genes and nuclear factor erythroid 2‑related factor (Nrf2) signaling. It was demonstrated that geniposide increased the viability of the Cd‑treated MC‑3T3‑E1 cells. Geniposide decreased apoptosis and ROS accumulation compared to these parameters in the Cd group. Geniposide attenuated oxidative stress‑related factors, malondialdehyde and lactate dehydrogenase and increased antioxidant key enzyme superoxidase dismutase (SOD). The expression levels of Bax, Bcl‑2 and survivin were modulated by geniposide. Additionally, the mRNA and protein expression of the receptor activator of NF‑κB ligand (RANKL) and osterix were significantly increased, while osteoprotegerin was decreased by geniposide treatment compared to the Cd groups. Geniposide also enhanced Nrf2, heme oxygenase‑1 (HO‑1) and NAD(P)H quinone dehydrogenase 1 (NQO1) expression. The present study identified a potential agent for the treatment of Cd‑induced osteoblast injury.