阿斯特拉加卢斯多糖增强O-GlcNAcylation通过OGT改善间脊椎盘退化在老鼠
Hao Tan1, Cao Fang2, Yiyun Tan1
1Department of Orthopedics, Changsha Hospital of Traditional Chinese Medicine (Changsha Eighth Hospital), Changsha, China.
Journal of cellular and molecular medicine
|December 10, 2025
概括
阿斯特拉加勒斯的多糖 (APS) 通过通过OGT.通过增强O-链接的β-N-乙糖胺修饰 (O-GlcNAcylation) 来防止椎间盘退化 (IVDD). 这一过程稳定了Nrf2,缓解了IVDD.
科学领域:
- 生物化学和分子生物学
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 阿斯特拉加勒斯多糖 (Astragalus polysaccharides,简称APS) 具有不同的药理活动.
- 异常的O-链接β-N-乙糖胺修饰 (O-GlcNAcylation) 与椎间盘退化 (IVDD) 有关.
- 在IVDD中调节O-GlcNAcylation中的APS的作用尚不清楚.
研究的目的:
- 在IVDD的背景下调查APS对O-GlcNAcylation的影响.
- 阐明APS影响O-GlcNAcylation和Nrf2表达的分子机制.
- 评估APS对IVDD的治疗潜力.
主要方法:
- 使用了分子对接,循环赫西米德追逐试验,免疫组织化学和免疫沉.
- 在体外研究中,涉及到暴露于 tert-butyl氧化物 (TBHP) 的核细胞 (NPC).
- 在体内研究使用IVDD的老鼠模型进行.
主要成果:
- 在TBHP诱导的NPC中,APS治疗增加了O-GlcNAcylation和O-GlcNAc转移酶 (OGT) 表达.
- APS恢复了NPC的活力,促进了原二和原蛋白的合成,并减少了亡.
- 通过促进OGT介导的O-GlcNAcylation,APS稳定了Nrf2的表达,抑制了无素-蛋白酶体通路.
结论:
- 通过OGT,APS促进O-GlcNAcylation,从而提高Nrf2的稳定性.
- 这种机制有助于APS对IVDD的保护作用.
- APS证明了缓解IVDD的治疗潜力.
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