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• 营养卫生 •    下一篇

肉苁蓉多糖影响肠道菌群抑制Toll样受体4/核因子κB途径改善小鼠糖尿病肾病

罗欣杰1,2,杨建华3,4,胡君萍4   

  1. 1.
    2. 新疆医科大学
    3. 新疆医科大学第一附属医院药学部
    4. 新疆医科大学药学院
  • 收稿日期:2024-04-16 修回日期:2024-08-30 出版日期:2024-11-15 发布日期:2024-11-01
  • 通讯作者: 胡君萍 E-mail:hjp_yxy@163.com
  • 作者简介:2024-07-15
  • 基金资助:
    新疆维吾尔自治区自然科学基金重点项目;新疆维吾尔自治区自然科学基金重点项目;新疆天然药物活性组分与释药技术重点实验室

Cistanche deserticola polysaccharides affect intestinal flora and inhibit TLR4 / NF-κB signaling pathway to improve diabetic nephropathy in mice

Xinjie Luo1,2, Jun-Ping HU   

  • Received:2024-04-16 Revised:2024-08-30 Online:2024-11-15 Published:2024-11-01
  • Contact: Jun-Ping HU E-mail:hjp_yxy@163.com

摘要: 摘 要:本研究旨在探究肉苁蓉多糖(cistanche deserticola polysaccharides,CDPs)对糖尿病肾病(diabetic nephropathy,DN)小鼠模型的改善作用及其可能机制。通过高糖高脂饮食结合STZ注射建立DN模型,将36只C57BL/6N雄性小鼠随机分组,给予CDPs不同剂量处理,持续4周。检测小鼠的生理指标、肾功能、炎症因子和肠道菌群变化。结果显示,CDPs显著改善DN小鼠的一般状态和肾脏病理结构,降低血糖、尿蛋白等指标,减少炎症因子和纤维化因子的水平。此外,CDPs影响肠道菌群平衡,增加有益菌丰度,降低潜在致病菌,改善肠道屏障功能。CDPs还抑制TLR4/NF-κB信号通路的活化,减少LPS的释放。综上,CDPs通过影响肠道菌群和抑制炎症信号通路,对DN小鼠模型表现出改善作用,为DN治疗提供了新的思路。

关键词: 肉苁蓉多糖, 糖尿病肾病, 肠道屏障, 肠道菌群, Toll样受体4, 核因子κB

Abstract: Abstract: The objective of this study is to investigate the ameliorative effects and potential mechanisms of Cistanche deserticola polysaccharides (CDPs) on a diabetic nephropathy (DN) mouse model. The DN model was established by administering a high-sugar, high-fat diet combined with intraperitoneal injection of streptozotocin (STZ). Thirty-six C57BL/6N male mice were randomly divided into groups and treated with different doses of CDPs for 4 weeks. Physiological indices, renal function, inflammatory factors, and intestinal microbiota changes were assessed. The results showed that CDPs significantly improved the general condition and renal histopathological structure of DN mice, reduced blood glucose, urinary protein, and levels of inflammatory and fibrotic factors. Additionally, CDPs affected the balance of the intestinal microbiota, increased the abundance of beneficial bacteria, decreased potential pathogenic bacteria, and improved intestinal barrier function. CDPs also inhibited the activation of the TLR4/NF-κB signaling pathway and reduced the release of lipopolysaccharide (LPS). In conclusion, CDPs exhibit ameliorative effects on the DN mouse model by affecting the intestinal microbiota and inhibiting inflammatory signaling pathways, offering new insights for the treatment of DN.

Key words: Cistanche deserticola polysaccharide, diabetic nephropathy, intestinal barrier, intestinal flora, Toll like receptor 4, nuclear factor κB