电针在子的膝关节骨关节炎中通过线粒细胞吸收途径产生冠状动脉保护作用
Longfei Xing1, Xilin Chen2,3, Changqing Guo1
1School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, People's of Republic of China.
Journal of pain research
|August 28, 2023
概括
电针 (EA) 通过激活线粒细胞吸收 (mitophagy) 来保护膝关节骨关节炎 (KOA) 软骨. 这一过程可以去除受损的线粒体,并通过Pink1-Parkin通路恢复平衡,从而保持状细胞的生存.
科学领域:
- 整形外科和再生医学
- 细胞生物学和线粒体动力学
- 骨关节炎病理生理学 病理生理学
背景情况:
- 软体细胞中的线粒体功能障碍是膝关节骨关节炎 (KOA) 进展的关键因素.
- 激活线粒细胞吸收,这是一种清除受损线粒体的细胞过程,对于状细胞的存活和软骨健康至关重要.
- 研究可以调节KOA中线粒细胞衰变的治疗干预措施是必不可少的.
研究的目的:
- 为了确定电针 (EA) 干预是否会激活胆红细胞中的髓.
- 在KOA.的子模型中探索米托法基在EA的软骨保护作用中的作用.
- 阐明分子通路,特别是Pink1-Parkin通路,参与EA介导的线粒.
主要方法:
- 使用修改的维德曼固定方法建立KOA子模型.
- 治疗KOA子用电 (EA) 每隔一天3周.
- 评估软骨退化,线粒体形态,ATP水平,和表达与线粒体相关的蛋白质 (LC3 II/I,TOM20,TIM23) 和Pink1-Parkin通路通过萨弗兰因O-快速绿色染色,免疫光学,传输电子显微镜,和西斑.
主要成果:
- 在KOA子中,EA治疗显著降低了软骨退化和增加了原II分布.
- EA激活了冠状细胞中的线粒细胞衰变,由LC3 II/I比率的增加和TOM20/LC3B的同位化证明.
- 通过降低TOM20和TIM23的积累和增加ATP的产生,EA恢复了线粒体平衡,可能是通过上调Pink1-Parkin通路.
结论:
- 电针 (EA) 在膝关节骨关节炎 (KOA) 中显示出显著的软骨保护作用.
- 由Pink1-Parkin途径介导的EA诱导的线粒是其治疗益处的关键机制.
- 通过EA针对mitophagy提供了一种有前途的治疗策略,通过保护状细胞功能和软骨完整性来管理KOA.
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