Liquiritin Exerts a Dual Effect on BMSCs Osteogenic Differentiation and Fracture Healing by Activating the ERK/JNK Pathway and Providing Antioxidant Protection

Abstract

Liquiritin, a flavonoid from Glycyrrhiza uralensis L., has diverse pharmacological properties, but its impact on fracture healing is unexplored. This study investigates its osteogenic and antioxidative effects on bone marrow mesenchymal stem cells (BMSCs) in vitro and its regenerative effect on rat femoral fractures in vivo. Cytotoxicity is assessed via MTT assay, and osteogenic differentiation via ALP and ARS staining. A rat femoral fracture model validates its therapeutic effects, with micro-CT and histological assessments evaluating healing outcomes. Gene and protein expression in osteogenic and signaling pathways are analyzed through RT-qPCR, western blot, and immunofluorescence. ROS levels are measured using DCFH-DA staining. Results show liquiritin enhances osteogenesis in BMSCs, evidenced by increased ALP activity and calcium deposition. In rats, it facilitates bone regeneration and upregulates phosphorylated ERK and JNK. Additionally, it reduces ROS generation post-oxidative injury, boosting NRF2, HO1, and NQO1 expression.