丹德罗的多糖化合物可以通过破坏KEAP1-NRF2相互作用的稳定性来预防葡萄糖皮质醇诱导的骨质疏松症
Yunjia Wang1, Zhongjing Jiang1, Linhua Deng1
1Department of Spine Surgery and Orthopaedics, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China.
International journal of biological macromolecules
|August 31, 2023
概括
丹德罗 officinale 多糖 (DOP) 在治疗葡萄糖皮质醇诱导的骨质疏松症 (GIOP) 中表现有前途. 通过调节Nrf2/Keap1通路,DOP可以防止骨质损失,并促进骨生长.
科学领域:
- 药理学和传统医学的医学.
- 骨生物学和骨质疏松症研究研究
背景情况:
- 葡萄糖皮质醇诱导的骨质疏松症 (GIOP) 是二次骨质疏松症和骨折的主要原因.
- 目前针对GIOP的治疗方法在安全性和成本方面存在局限性,需要新的治疗策略.
- 传统中医药中的Dendrobium officinale已经证明对骨代谢有潜在的益处.
研究的目的:
- 调查Dendrobium officinale多糖 (DOP) 对GIOP的治疗作用.
- 在用德克萨米他治疗的模型中探索DOP作用的潜在分子机制.
主要方法:
- 在体内研究使用斑马鱼和小鼠模型的GIOP诱导德甲 (DEX).
- 在体外实验中使用与DEX治疗的人类骨髓衍生干细胞 (hBMSCs).
- 研究Nrf2/Keap1通路,包括Nrf2核转移,无处不在和相互作用破坏,使用淘汰和RNAi技术.
主要成果:
- 在体外和体内,低度的DOP被认为是安全的.
- 在斑马鱼和小鼠模型中,DOP治疗显著改善了DEX诱导的骨质疏松症.
- 通过抑制Nrf2无处不在,DOP增强了DEX处理的hBMSC的骨质分化,并提高了核Nrf2水平.
- 证明DOP会破坏Nrf2/Keap1的相互作用,从而导致Nrf2的稳定.
结论:
- 丹德罗 officinale 多糖 (DOP) 显示出对抗葡萄糖皮质类药物诱导的骨质疏松症具有显著的治疗潜力.
- 在葡萄糖皮质类药物的存在下,DOP通过破坏Nrf2/Keap1相互作用来刺激骨质生成.
- DOP代表了一种有前途的新型治疗剂,用于管理GIOP.
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