虹膜素通过抑制脂肪细胞中通过TLR4/MyD88/NF-κB轴的干扰来缓解因肥胖引起的骨质损失

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Yuanshu Zhang¹, Xu He², Kai Wang¹

¹Department of Orthopedics, Wuxi Ninth People's Hospital Affiliated to Soochow University, Wuxi, Jiangsu 214026, PR China; Department of Orthopedics, The First Affiliated Hospital of Soochow University, Orthopedics Institute of Soochow University, Suzhou, Jiangsu 215006, PR China.

Journal of advanced research

|April 16, 2024

概括

一种肌素的虹膜素通过抑制脂肪细胞分化和通过TLR4/MyD88/NF-κB通路减少互白素-6 (IL-6) 来缓解肥胖引起的骨质损失,从而增强骨形成.

科学领域:

内分泌学和新陈代谢学
骨生物学和骨质疏松症研究研究
脂肪细胞生物学和信号传递

背景情况:

肥胖是一个全球性的健康问题,与骨质降低和骨质疏松症有关.
素,一种由纤维素第3类域含蛋白5 (FNDC5) 衍生出来的肌素,影响骨和脂肪代谢.
素在骨髓微环境中调解肥胖对骨代谢的影响中的作用需要阐明.

研究的目的:

通过研究虹膜素对骨代谢的影响,特别是通过其对脂肪细胞的影响.
在肥胖的背景下,探索虹膜素影响骨髓中介质干细胞 (BMSCs) 差异化的机制.

主要方法:

使用的纤维素第3类域含蛋白5 (FNDC5) 淘汰赛小鼠接受高脂肪饮食 (HFD),并通过微型CT和组织学评估骨质量.
试验室研究涉及评估骨髓介质干细胞 (BMSCs) 的脂原和骨原分化.
使用RNA测序和确认的信号通路 (TLR4/MyD88/NF-κB) 分析了差异化脂肪细胞中的基因表达,并采用了西斑和qRT-PCR.

主要成果:

与标准饮食对照相比,高脂肪饮食养的FNDC5淘汰赛小鼠表现出体重增加,骨髓脂肪增加和骨形成减少.
在体外,虹膜素抑制了BMSC分化成脂肪细胞,并挽救了由脂肪细胞超位抑制的骨质生成.
虹膜素通过TLR4/MyD88/NF-κB通路降低脂肪细胞中介素-6 (IL-6) 的产生,在HFD养的FNDC5淘汰赛小鼠中观察到IL-6的增加.

结论:

虹膜素通过降低TLR4/MyD88/NF-κB通路的调节和减少脂肪细胞中IL-6的产生来增强BMSC的骨质生成.
准伊丽素对脂肪细胞衍生的IL-6的调节,为肥胖引起的骨质疏松症提供了潜在的治疗策略.
这项研究强调了虹膜素对高脂肪饮食引起的骨质损失的保护作用.

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