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斯基桑德罗B通过向TRAF6-NOX1通路来抑制骨质细胞形成并减轻雌激素缺乏引起的骨损失

Yuangang Su¹, Jiamin Liang¹, Haoyu Lian¹

¹Guangxi Key Laboratory of Regenerative Medicine, Orthopaedic Department, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China; Collaborative Innovation Centre of Regenerative Medicine and Medical BioResource Development and Application Co-constructed by the Province and Ministry, Life Sciences Institute, Guangxi Medical University, Nanning, Guangxi, 530021, China.

Phytomedicine : international journal of phytotherapy and phytopharmacology

|December 23, 2025

概括

斯基桑德罗B (SolB) 通过减少氧化应激和向关键信号通路,有效地抑制骨质细胞形成和骨再吸收. 这种天然化合物在骨质疏松症模型中有望预防骨质损失.

科学领域:

生物化学生物化学
药理学药理学是指药理学的学科.
骨生物学骨生物学骨生物学

背景情况:

骨质疏松症的特点是骨质细胞活性增加和骨质再吸收.
向骨质细胞生成是骨质疏松症治疗的关键策略.
斯基桑德罗B (SolB) 对骨质细胞和骨质疏松症的影响尚不清楚.

研究的目的:

为了研究SolB对骨质细胞的抑制作用.
确定SolB在预防雌激素缺乏引起的骨质疏松症方面的有效性.

主要方法:

在实验室测试中评估了骨质细胞生成,F-actin环形成,骨再吸收,细胞内活性氧物种 (ROS) 和抗氧化酶.
转录组分析确定了SolB对RANKL介导的信号通路的影响.
分子对接,动力学和表面等离子体共振 (SPR) 证实了SolB与标蛋白结合.
一个卵巢切除 (OVX) 的小鼠模型评估了SolB对骨质的保护作用.

主要成果:

SolB通过增强抗氧化酶,减少细胞内ROS,Ca2+和NFATc1表达来抑制骨质细胞的产生和骨质再吸收.
SolB抑制了RANKL诱导的TRAF6-NF-κB和MAPK信号通路的激活.
SPR证实了SolB与TRAF6和NOX1.1的结合.
通过减少NOX1的表达和增加抗氧化酶的表达,SolB治疗保护了OVX小鼠的骨质损失.

结论:

SolB显示出作为预防和治疗绝经后骨质疏松症的有效治疗剂的潜力.
SolB的机制涉及调节氧化应激和关键信号通路,涉及骨质细胞形成.

关键词:

在NOX1中,NOX1是骨质细胞是骨质结晶体.骨质疏松症是一种骨质疏松症.斯基桑德罗尔 B 类药物在TRAF6中,

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