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Browsing by Subject "Osteoclastogenesis"

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    Puerarin and zinc additively prevent mandibular bone loss through inhibiting osteoclastogenesis in ovariectomized rats
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Liu, Hao; Li, Wei; Jia, Shengnan; Li, Binbin
    Puerarin and zinc play a key role in preventing osteoporotic-related bone loss. Previous research on puerarin or zinc mainly focused on the antiosteoporotic effects of long bone. However, it is obscure for puerarin or zinc to prevent mandibular osteoporosis. Here, we explore the effects on additive coadministration of puerarin and zinc on preventing mandibular bone loss in ovariectomized rats, and evaluate the underlying mechanisms ex vivo. Rats were ovariectomized and administrated puerarin, zinc or both. After 12 weeks, bone mineral density (BMD) and histomorphometry of mandibles were measured by micro-CT. The mechanical properties were determined using a threepoint bending test. Then, osteogenic differentiation of primary bone marrow stromal cells (BMSCs) and osteoclastogenesis of bone marrow mononuclear were performed ex vivo. The culture supernatant and serum level of bone biochemical markers including osteoprotegerin (OPG), osteopontin (OPN), receptor activator of nuclear factor (NF)-κB ligand (RANKL), and tartrate-resistant acid phosphatase (TRAP) were detected by ELISA. Culture supernatant and serum levels of calcium were measured using a Plasma Emission Spectrometer. One-way ANOVA was used for statistical analyses. The results showed that administration of puerarin plus zinc prevented the decrease in mandibular BMD and bone morphometrical parameters more effectively than single use of puerarin or zinc (p<0.05), which was similar to the biomechanical tests (p<0.05). Furthermore, puerarin and zinc additively up-regulated OPG, OPN protein levels, Ca ion level and down-regulated RANKL, TRAP protein levels. In conclusion, puerarin and zinc additively prevent mandibular bone loss through inhibiting osteoclastogenesis in ovariectomized rats, which will shed more light on the potential use of puerarin and zinc in the prevention/treatment of oral bone loss clinically.
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    Resistant dextrin protects against pathological bone loss in ovariectomized rats and inhibits RANKL-induced osteoclastogenesis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Wang, Hongwei; Bu, Xiaojie; Chen, Fulian; Wang, Yan; Chen, Yao
    Background. Osteoporosis is a common disease in postmenopausal women characterized by systemic bone mass loss, microstructure fragility and increased incidence of fractures. Resistant dextrin (RD) is a soluble fiber with beneficial metabolic effects. However, the beneficial effect of RD in osteoporosis remains to be determined. Methods. In this study, we investigated the effect of dietary RD supplement on osteoporosis in ovariectomized (OVX) rats. Both the control (sham) and OVX group rats were gavaged with RD (10 g/kg/d) or equal amount of saline for 12 weeks, and histological and biomechanical analyses were conducted to evaluate bone microstructure and strength. Furthermore, we also evaluated the effects of RD on osteoclastogenesis in bone marrow macrophages (BMMs) by detecting the expression of osteoclast-related genes using qRT-PCR and Western blot analysis. Results. The results showed that in OVX rats the bone strength and microstructure characteristics were significantly improved with RD supplement for 12 weeks. Additionally, the mRNA and protein expression of osteoclast markers, such as CTSK, NF-κB and NFATC1, were significantly down-regulated in BMMs isolated from RD supplement group. RD also suppressed RANKL-induced osteoclastogenesis in BMMs. Conclusion. These findings suggest that RD ameliorates osteoporosis in OVX rats by inhibiting osteoclast differentiation. RD suppresses RANKLinduced osteoclastogenesis possibly through modulating Akt and NF-κB signaling pathways. These data indicate that a dietary supplement of RD might serve as an intervention strategy for menopausal osteoporosis

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