Quercus salicina Blume Inhibits Bone Loss via Dual Effects on Osteoblasts and Osteoclasts
Suhyun Cho, Nadzeya Lazerka, Soyeon Hong, Minji Gwon, Byeong Jun Jeon, Jeong Do Kim, Gyhye YooBackground/Objectives: Osteoporosis is a progressive metabolic bone disorder with reduced bone mass and microarchitectural deterioration, leading to an increased risk of fractures. With an aging population, there is a growing demand for safe and effective long-term therapeutic methods for osteoporosis and medicinal plants could be promising candidates as novel agents for osteoporosis. In this study, we investigated the effects of the 70% ethanol extract of Quercus salicina Blume (QS), an herbal plant, on osteoporosis. Methods: MC3T3-E1 mouse pre-osteoblast cells and RAW264.7 mouse macrophage cells were utilized to assess osteoblast and osteoclast differentiation, respectively. QSEE (10 mg/kg and 40 mg/kg) was orally administered for 12 weeks in OVX mice, a postmenopausal osteoporosis animal model, and bone parameters were evaluated using Micro-Computed Tomography (Micro-CT). Ex vivo experiments were conducted using primary cells isolated from mouse femurs and tibias. Expression levels of proteins and mRNAs related to osteoblasts and osteoclasts were estimated by Western blot and Quantitative Real-Time PCR (qRT-PCR). Results: QSEE showed osteogenic activity by increasing alkaline phosphatase (ALP) activity, protein and mRNA expression related to osteoblast differentiation. QSEE decreased osteoclast differentiation by suppressing tartrate-resistant acid phosphatase (TRAP) activity, protein and mRNA expression related to osteoclast differentiation. In OVX mice, QSEE administration restored bone microarchitecture decreased by OVX. In primary cells isolated from mouse femurs, QSEE increased osteoblast-related markers and decreased osteoclast-related markers. Conclusions: These findings suggest Quercus salicina Blume has potential as an anti-osteoporosis agent by inducing osteoblast differentiation and suppressing osteoclast differentiation.