通过ROS介导的线粒和亡调节MLO-Y4细胞中TCP颗粒引起的骨细胞死亡
Pei Yang1, Bingbing Xu1, Ruirong Zhu1
1College of Medicine, Shaoxing University, Huancheng West Road 508, Shaoxing 312000, PR China.
Toxicology
|September 7, 2023
概括
三酸 (TCP) 颗粒通过诱导菌和亡,由活性氧物种 (ROS) 介导的过程触发骨细胞死亡. 这种细胞死亡有助于周围假肢骨解和植入物失败.
科学领域:
- 生物材料科学 生物材料科学
- 细胞生物学 细胞生物学
- 整形外科的研究研究.
背景情况:
- 骨细胞细胞死亡有助于周围假肢骨解,关节松和植入物失败.
- 三酸 (TCP) 颗粒诱导骨细胞死亡的确切机制尚不清楚.
研究的目的:
- 阐明TCP粒子诱导的骨细胞死亡背后的机制.
- 在这个过程中调查线粒,亡和氧化应激的作用.
主要方法:
- 使用了暴露于TCP粒子的MLO-Y4骨质细胞系.
- 评估了细胞活力,线粒体功能,自标志物 (LC-3 II,帕金,PINK1,p62),亡标志物 (RIP1,RIP3,MLKL),活性氧物种 (ROS) 生产以及相关的信号通路.
- 在机械学研究中使用自抑制剂 (Baf A1),亡抑制剂 (Nec-1,NSA) 和ROS清除剂 (NAC).
主要成果:
- TCP颗粒降低了骨细胞活力,并诱导了线粒体损伤.
- TCP颗粒显著增加了自流,线粒和亡,由升高的LC-3 II,帕金,PINK1和化RIP1/RIP3/MLKL证明.
- TCP粒子增加了细胞内和线粒体ROS,增加了TXNIP,减少了抗氧化蛋白 (TRX1,Nrf2,HO-1,NQO1),表明氧化应激.
- 在ROS清理过程中逆转了TCP诱导的线粒和亡.
- 抑制线粒和亡缓解了骨细胞死亡和随后的骨质细胞形成.
结论:
- 反应性氧物种 (ROS) 通过食和亡的联合途径调解TCP粒子诱导的骨细胞死亡.
- 了解这些机制,可以深入了解周围假肢骨解和潜在的治疗点.
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