Crocin alleviates the steroid-induced osteonecrosis of the femoral head injuries via ROS-mediated JNK/c-Jun signaling pathway

Objective: To explore the role and functional mechanism of crocin in glucocorticoids induced osteonecrosis of the femoral head (ONFH). Methods: Primary osteoblasts from rat were stimulated with dexamethasone and treated with crocin in different doses and reactive oxygen species (ROS) inhibitor in vitro. Cell viability and cell apoptosis rate were assayed by cell counting kit-8 and flow cytometry, respectively. The level of alkaline phosphatase activity, ROS and mitochondrial membrane potential were detected by ELISA. The expression of related proteins was detected via Western blot. As for in vivo study, 30 rats were equally grouped into control group, ONFH model group (steroid-induced ONFH) and crocin treatment group. The occurrence and histopathological changes of ONFH, bone tissue cell apoptosis, and bone microstructure and loss were analyzed. Results: In vitro experiments, crocin and ROS inhibitor could reverse the reduction of cell viability, differentiation and mitochondrial membrane potential content, as well as the increase of ROS production, apoptosis rate and the expression levels of p-JNK and p-c-Jun in primary osteoblasts caused by dexamethasone. In vivo experiments, compared with rats in the control group, ONFH model rats had decreased amount of femoral head bone and the integrity of bone tissues, but aggravated apoptosis rate of femoral head cells and empty trabecular; however, crocin treatment significantly improved these microstructures of femoral head bone. Conclusion: Crocin had a favorable therapeutic effect on steroid-induced ONFH in rats by ROS/JNK/c-Jun pathway.