阿斯特拉加卢斯多糖化物通过抑制TLR4/NF-κB通路,改善糖尿病病患者的炎反应
Mingfei Guo1,2, Jiarong Gao3, Lei Jiang4
1Department of Scientific Research, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.
Drug design, development and therapy
|July 25, 2023
概括
阿斯特拉加卢斯多糖 (APS) 通过减少炎症和抑制TLR4/NF-κB通路,有效治疗糖尿病病 (DN). 这项研究探讨了APS.
科学领域:
- 药理学和毒理学 药理学和毒理学
- 腎臟病學 (nephrology) 是一種醫學.
- 免疫学 免疫学 免疫学
背景情况:
- 糖尿病病 (DN) 是糖尿病的严重并发症,导致末期病.
- 阿斯特拉加卢斯多糖 (Astragalus polysaccharide,简称APS) 是一种来自Astragalus membranaceus的多糖,用于治疗糖尿病.
- 在DN中APS的抗炎机制尚未完全理解.
研究的目的:
- 调查APS改善糖尿病病炎症的分子机制.
- 在体内 (老鼠模型) 和体内 (球状细胞) 的DNA模型中探索APS的影响.
主要方法:
- 采用了链毒素 (STZ) 诱导的DN大鼠模型和高葡萄糖 (HG) 处理的质细胞模型.
- 评估的禁食血糖 (FBG),/体重比,血清肌素 (Scr),血液尿素 (BUN) 和24小时尿蛋白.
- 评估了病理 (HE染色),炎症性细胞因子 (IL-1β,IL-6,MCP-1通过ELISA),细胞增殖 (CCK-8,流细胞计),以及TLR4/NF-κB通路激活 (qRT-PCR,西部斑).
主要成果:
- 在DN大鼠中,APS治疗显著降低了FBG,BUN,Scr和病理损伤.
- 通过降低IL-1β,IL-6,MCP-1水平并抑制TLR4/NF-κB通路,APS改善了损伤.
- 在体外,APS减轻了HG诱导的炎症和球细胞中的增殖.
结论:
- 阿斯特拉加卢斯多糖 (APS) 显示出对糖尿病病 (DN) 损伤的保护作用.
- APS通过减轻炎症反应来发挥其治疗作用.
- APS的抗炎机制涉及TLR4/NF-κB信号通路的减弱.
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