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阿波基因因通过Nrf2信号通路抑制氧化应激,对德克萨米他诱导的骨质母细胞产生细胞保护作用

Xinglong Zhang¹, Ran Pang¹, Kai Zhang²

¹Department of Orthopaedics, TianjinNankai Hospital, Tianjin, China.

Journal of cellular and molecular medicine

|September 26, 2023

概括

亚波基尼 (APO) 通过改善骨质细胞存活率和恢复线粒体功能,防止类固醇诱导的股骨头亡. 这通过激活Nrf2通路来实现,为这种情况提供了潜在的治疗方法.

科学领域:

生物医学科学生物医学科学
药理学药理学是指药理学的学科.
整形外科整形外科整形外科

背景情况:

类固醇诱导的股骨头亡 (SIFHN) 是葡萄糖皮质醇 (GC) 治疗的严重并发症.
GCs诱导骨质细胞亡和线粒体功能障碍,有助于SIFHN.
作为一种抗氧化剂和抗瘤化合物的阿波基尼 (APO) 已经显示出有前途.

研究的目的:

调查APO对SIFHN的保护作用.
阐明APO作用的潜在分子机制.

主要方法:

在体外研究使用德克萨米他 (Dex) 治疗的骨质细胞来评估细胞活力,氧化应激 (OS) 和线粒体功能.
使用SIFHN.的老鼠模型进行体内研究.
通过使用ML385来阻止Nrf2.2,研究了Nrf2通路的作用.

主要成果:

低剂量的APO没有对骨质母细胞表现出任何毒性.
在用Dex治疗的细胞中,APO改善了骨质细胞存活率,抑制了OS,并恢复了线粒体功能.
APO激活了Nrf2通路,这对其保护作用至关重要,因为阻断Nrf2取消了益处.
在体内,APO减少了空隙,恢复了骨质,并在SIFHN大鼠中增加了Nrf2表达.

结论:

通过Nrf2通路的激活,APO保护骨质细胞免受德克萨诱导的氧化应激和线粒体功能障碍.
APO显示出作为治疗类固醇诱导的股骨头缩症的治疗剂的潜力.

关键词:

Nrf2 路径的路径这就是Apocynynyn.腿部头部亡的死亡.骨质细胞的亡是骨质细胞的亡.氧化应激是一种氧化应激.

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