辅酶Q10通过调节miR-130b-3p/PGC-1α通路来改善线粒体功能,防止高脂血症诱导的骨质疏松症
Meng Meng1, Jiaying Wang2, Changyuan Wang2
1Department of Orthopaedics, First Affiliated Hospital, Dalian Medical University, No. 222, Zhongshan Road, Xigang District, Dalian, 116011, China.
Calcified tissue international
|December 6, 2023
概括
辅酶Q10 (CoQ10) 通过改善线粒体功能和平衡骨细胞分化来逆转超脂血症诱导的骨质疏松症. 这项研究揭示了CoQ10的存在.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 代谢性骨疾病 代谢性骨疾病
背景情况:
- 超脂血症通过促进骨髓中介酶干细胞 (BMSCs) 的骨质生成,促进脂肪生成,从而导致骨质疏松症.
- 氧化应激和线粒体功能障碍与高脂血症引起的骨质损失有关.
- 共酶Q10 (CoQ10) 是一种线粒体抗氧化剂,但其在超脂血症相关的骨质疏松症中的作用尚未被探索.
研究的目的:
- 研究辅酶Q10对高脂血症诱导的骨质疏松症的治疗作用和机制.
- 为了阐明CoQ10如何影响BMSCs在超脂血症条件下的脂肪细胞-骨质母细胞血统分配.
主要方法:
- 利用高脂肪饮食 (HFD) 养的ApoE-/-小鼠和氧化低密度脂蛋白 (ox-LDL) 治疗的BMSC来模拟超脂血症诱导的骨质疏松症.
- 评估血清脂质水平,骨形成标记物,线粒体功能 (ATP含量,ROS生成) 和PGC-1α表达.
- 在BMSC中进行了PGC-1α倒置和miR-130b-3p抑制剂治疗的体外实验.
主要成果:
- 在HFD养的ApoE/-小鼠和牛LDL治疗的BMSC中,CoQ10治疗逆转了血清脂水平升高和骨形成标记物降低.
- 在模型中,CoQ10对抗降低了PGC-1α表达,线粒体功能障碍,减少了ATP和增加了活性氧物种 (ROS).
- 抑制PGC-1α加剧了ROS,BMSC亡和脂肪生成,同时抑制了骨质生成;miR-130b-3p抑制增加了PGC-1α和改善了线粒体功能.
结论:
- 辅酶Q10通过调节脂肪细胞-骨质细胞系分配,有效地缓解了ApoE-/-小鼠的超脂血症诱导的骨质疏松症.
- 辅酶Q10的治疗机制包括通过调节miR-130b-3p/PGC-1α通路来增强线粒体功能.
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