ArticleBMC musculoskeletal disorders2025
YS-49 activates the PI3K/AKT signaling pathway in MC3T3-E1 cells to enhance osteoblast differentiation and inhibits glucocorticoid-induced bone loss in vivo.
Article in BMC musculoskeletal disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Abstract
backgroundGlucocorticoid-induced osteoporosis (GIOP) is a bone disorder marked by decreased bone density and an elevated risk of fracture. The Phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway plays a pivotal role in regulating osteoblast proliferation and differentiation, serving as a central molecular mechanism in bone homeostasis and making it a potential therapeutic target for GIOP. YS-49, an l-naphthylmethyl analog of higenamine, has demonstrated that it can influence various cellular processes through activating the PI3K/AKT signaling pathway.This study investigated the role and mechanism of YS-49 in osteoblast differentiation.
methodsMC3T3-E1 cells were utilized to evaluate cell viability, apoptosis, reactive oxygen species (ROS) levels, malondialdehyde (MDA), superoxide dismutase (SOD) levels, Determinationosteogenic differentiation, and mineralization after treatment with YS-49 and dexamethasone (Dex). Osteogenic differentiation of MC3T3-E1 cells was assessed by Western blot and alkaline phosphatase (ALP) staining, with the former specifically analyzing YS-49-induced activation of the PI3K/AKT signaling pathway. Additionally, a GIOP mouse model was established, and the therapeutic effects of YS-49 were evaluated via bone mineral density (BMD), micro-computed tomography (micro-CT), enzyme linked immunosorbent assay (ELISA), and histopathological analysis.
resultsYS-49 enhanced cell viability, inhibited ROS production, and suppressed apoptosis in Dex-treated MC3T3-E1 cells. Moreover, it promoted osteogenic differentiation and mineralization by activating the PI3K/AKT signaling pathway. In vivo, YS-49 treatment significantly mitigated Dex-induced bone loss, as evidenced by the increased BMD, enhanced trabecular structure, and upregulation of the expression of osteogenic markers.
conclusionYS-49 promotes osteogenesis and prevents glucocorticoid-induced bone loss by activating the PI3K/AKT signaling pathway, collectively positioning it as a promising novel therapeutic agent for GIOP treatment.
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