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三叶豆紫檀苷通过抑制破骨细胞分化和骨吸收来保护去卵巢诱导的小鼠骨质流失。

Trifolirhizin protects ovariectomy-induced bone loss in mice by inhibiting osteoclast differentiation and bone resorption.

作者信息

Lin Zihong, Zhou Zhigao, Ye Jiajie, Wei Jinfu, Chen Shaozhe, Zhou Wenyun, Bi Yonghao, Zhou Zibin, Xie Gang, Yuan Guixin, Yao Guanfeng

机构信息

Department of Orthopedics, The Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China.

Department of Shantou Central Hospital, Shantou, Guangdong, China.

出版信息

Heliyon. 2024 Jul 6;10(14):e34250. doi: 10.1016/j.heliyon.2024.e34250. eCollection 2024 Jul 30.

DOI:10.1016/j.heliyon.2024.e34250
PMID:39130482
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11315080/
Abstract

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 . Bone loss model was established by ovariectomy(OVX) in mice .

RESULTS

Trifolirhizin repressed osteoclastogenesis, bone resorption induced by receptor activator of nuclear factor kappa B ligand (RANKL) . Mechanistically, trifolirhizin inhibits RANKL-induced MAPK signal transduction and NFATc1 expression. Moreover, trifolirhizin inhibited osteoclast marker gene expression, including . 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.

摘要

背景

骨质疏松症是一种使人衰弱的病症,其特征在于骨密度和骨微结构降低,导致骨折易感性增加和死亡率上升,尤其是在老年人中。尽管有用于骨质疏松症治疗的药物,但仍需要具有更少副作用的靶向性和创新性药物。三叶豆紫檀苷是一种从苦参根中提取的天然蝶豆素,此前已对其某些抗癌和抗炎作用进行了研究。三叶豆紫檀苷对破骨细胞形成和功能的影响尚不清楚。

目的

本文探讨了三叶豆紫檀苷在破骨细胞形成和功能中的可能作用及其潜在机制。方法:采用骨髓来源的巨噬细胞(BMMs)来评估三叶豆紫檀苷对破骨细胞生成、骨吸收及其潜在机制的作用。通过卵巢切除(OVX)建立小鼠骨质流失模型。

结果

三叶豆紫檀苷抑制破骨细胞生成以及核因子κB受体活化因子配体(RANKL)诱导的骨吸收。机制上,三叶豆紫檀苷抑制RANKL诱导的丝裂原活化蛋白激酶(MAPK)信号转导和活化T细胞核因子c1(NFATc1)表达。此外,三叶豆紫檀苷抑制破骨细胞标志物基因表达,包括……。另外,发现三叶豆紫檀苷可预防卵巢切除(OVX)诱导的小鼠骨质流失。

结论

三叶豆紫檀苷可有效抑制破骨细胞生成和骨吸收活性。我们的研究结果为三叶豆紫檀苷作为预防和治疗骨质疏松症及其他溶骨性疾病的潜在药物提供了证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/6bb4b6258d92/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/471893be8c7d/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/b180583677e4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/971fda769276/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/7404afa90eae/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/e4547e180691/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/6bb4b6258d92/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/471893be8c7d/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/b180583677e4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/971fda769276/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/7404afa90eae/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/e4547e180691/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/979f/11315080/6bb4b6258d92/gr5.jpg

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