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阿斯特拉加勒斯多糖-D1的结构特征及其通过丰富Staphylococcus lentus来改善低剂量甲福林的效果

Jianglan Long¹, Meng Li², Chengcheng Yao¹

¹Beijing Institute of Clinical Pharmacy, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, PR China.

International journal of biological macromolecules

|June 4, 2024

概括

阿斯特拉加卢斯多糖 APS-D1 增强了2型糖尿病的低剂量甲福林. 这种组合改善了肠道细菌,产生了l-卡尼,这促进了脂肪酸的氧化,降低了葡萄糖的生产,以更好地管理糖尿病.

科学领域:

药理学药理学是指药理学的学科.
微生物学微生物学
生物化学生物化学

背景情况:

低剂量甲胺是2型糖尿病的常见治疗方法.
寻求辅助疗法来提高甲福明的疗效并减少副作用.
阿斯特拉加勒斯膜是传统的药用草本,具有潜在的治疗性质.

研究的目的:

研究一种来自Astragalus membranaceus (APS-D1) 的同质多糖的潜力,作为2型糖尿病中低剂量甲福明的辅助疗法.
阐明APS-D1的作用机制,包括其对肠道微生物群和宿主新陈代谢的影响.

主要方法:

通过使用DEAE-52纤维素和Sephadex G-100染色学,从Astragalus membranaceus中净化APS-D1.
使用分子量分布,单糖化合物组成,红外光谱,甲基化分析和NMR来描述APS-D1结构.
在体内评估APS-D1对炎症的影响及其与低剂量甲福林的联合治疗.
对肠道细菌组成和代谢物 (l-carnitine) 产生的分析,以应对APS-D1治疗.
评估由组合疗法影响的代谢途径,包括脂肪酸氧化和葡萄糖生成.

主要成果:

APS-D1是一种7.36kDa的多糖,主要由葡萄糖,银河糖和阿拉比诺糖组成,经过净化和表征.
APS-D1显著改善了炎症标志物 (TNF-α,LPS,IL-10) 并增强了低剂量甲福明的治疗效果,没有任何不良事件.
组合疗法调节了肠道细菌,特别是丰富了生产l-carnitine的Staphylococcus lentus.
发现S. lentus和l-carnitine可以改善糖尿病,而它们的减少会损害治疗效果.
组合疗法促进了脂肪酸氧化 (CPT1) 和抑制葡萄糖生成 (PCK,G6Pase),由S. lentus和l-carnitine介导.

结论:

在2型糖尿病治疗中,APS-D1充当低剂量甲胺的有效辅助剂.
治疗效益通过丰富S. lentus和随后的l-carnitine生产来介导,从而影响关键的代谢途径.
这种组合策略为管理2型糖尿病提供了一个有希望的方法.

关键词:

阿斯特拉加勒斯的多糖化物.低剂量的甲福尔明.葡萄球杆菌 (Staphylococcus lentus) 已经被发现.结构性表征结构性表征

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