Osteoporosis is a systemic bone metabolism disorder, which increases the risk of fractures, and in severe cases it may cause disability or even death. An important factor contributing to
osteoporosis is the imbalance between bone formation and resorption.
Naringin was reported to promote osteoblast differentiation, thus enhancing bone formation and alleviating
osteoporosis development. However, the signalling pathways related to the regulatory mechanism of
naringin in
osteoporosis development are not clear. Proliferation of bone mesenchymal stem cells (BMSCs) treated with
naringin in vitro was detected by
CCK-8. An osteogenesis differentiation medium supplemented with
naringin was applied to explore the effects of
naringin on BMSC osteogenic differentiation, as detected by
Alizarin red staining.
Ovariectomy (OVX)-induced
postmenopausal osteoporosis (PMOP) rats were orally administered with
naringin. Dual-energy X-ray absorptiometry (DEXA) and micro-CT were applied to measure bone mineral density (BMD), bone volume/total volume (BV/TV), trabecula thickness (Tb.Th), trabecula number (Tb.N), trabecular separation (Tb.Sp) and bone surface/bone volume (BS/BV). H&E staining was performed to show pathological changes of the femur in PMOP rats after
naringin treatment. Bone metabolism indicators were assessed by ELISA. We found that
naringin suppressed the activation of the JAK2/STAT3 pathway.
Naringin promoted BMSC proliferation and osteogenic differentiation. Furthermore,
naringin alleviates bone loss and improves abnormal bone metabolism of PMOP rats. Collectively,
naringin promotes BMSC osteogenic differentiation to ameliorate
osteoporosis development by targeting JAK2/STAT3 signalling.