دورية أكاديمية
Trifolirhizin protects ovariectomy-induced bone loss in mice by inhibiting osteoclast differentiation and bone resorption
العنوان: | Trifolirhizin protects ovariectomy-induced bone loss in mice by inhibiting osteoclast differentiation and bone resorption |
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المؤلفون: | Zihong Lin, Zhigao Zhou, Jiajie Ye, Jinfu Wei, Shaozhe Chen, Wenyun Zhou, Yonghao Bi, Zibin Zhou, Gang Xie, Guixin Yuan, Guanfeng Yao |
المصدر: | Heliyon, Vol 10, Iss 14, Pp e34250- (2024) |
بيانات النشر: | Elsevier, 2024. |
سنة النشر: | 2024 |
المجموعة: | LCC:Science (General) LCC:Social sciences (General) |
مصطلحات موضوعية: | Trifolirhizin, Osteoclast differentiation, Osteoporosis, Osteoclast, MAPK-NFAT signaling pathway, Science (General), Q1-390, Social sciences (General), H1-99 |
الوصف: | Background: Osteoporosis is a debilitating condition characterized by reduced bone density and microstructure, leading to increased susceptibility to fractures and increased mortality, particularly among older individuals. Despite the availability of drugs for osteoporosis treatment, the need for targeted and innovative agents with fewer adverse effects persists. Trifolirhizin, a natural pterostalin derived from the root of Sophora flavescens, has been previously studied for its effects on certain anticancer and antiinflammatory. The impact of trifolirhizin on the formation and function of osteoclasts remain unclear. Purpose: Herein, the possible roles of trifolirhizin the formation and function of osteoclasts and the underlying mechanism were explored. Methods: Bone marrow-derived macrophages (BMMs) were employed to evaluate the roles of trifolirhizin on steoclastogenesis, bone absorption and the underlying mechanism in vitro. Bone loss model was established by ovariectomy(OVX) in mice in vivo. Results: Trifolirhizin repressed osteoclastogenesis, bone resorption induced by receptor activator of nuclear factor kappa B ligand (RANKL) in vitro. Mechanistically, trifolirhizin inhibits RANKL-induced MAPK signal transduction and NFATc1 expression. Moreover, trifolirhizin inhibited osteoclast marker gene expression, including NFATc1, CTSK, MMP9, DC-STAMP, ACP5, and V-ATPase-D2. Additionally, trifolirhizin was found to protect against ovariectomy(OVX)-induced bone loss in mice. Conclusion: Trifolirhizin can effectively inhibit osteoclast production and bone resorption activity. The results of our study provide evidence for trifolirhizin as a potential drug for the prevention and treatment of osteoporosis and other osteolytic diseases. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 2405-8440 |
Relation: | http://www.sciencedirect.com/science/article/pii/S2405844024102812; https://doaj.org/toc/2405-8440 |
DOI: | 10.1016/j.heliyon.2024.e34250 |
URL الوصول: | https://doaj.org/article/69c32deef9ac4d1fa64f82e8c49de67d |
رقم الأكسشن: | edsdoj.69c32deef9ac4d1fa64f82e8c49de67d |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 24058440 |
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DOI: | 10.1016/j.heliyon.2024.e34250 |