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

Cistanche deserticola Polysaccharides Attenuates Diabetic Nephropathy in Mice by Affecting the Intestinal Flora and Inhibiting the Toll-Like Receptor 4/Nuclear Factor-κB Signaling Pathway

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链霉佐菌素注射建立DN模型,将36只C57BL/6N雄性小鼠随机分组,实验组给予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可显著改善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,减少炎症因子的水平。此外,CDPs可影响肠道菌群平衡,通过增加有益菌相对丰度、降低潜在致病菌、改善肠道屏障功能。CDPs还可抑制Toll样受体4/核因子-κB信号通路的活化,减少脂多糖的释放。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,结果可为DN治疗提供新的思路。

The objective of this study was to investigate the ameliorative effect and potential mechanism of Cistanche deserticola polysaccharides(CDPs)on diabetic nephropathy(DN)in mice.The DN mouse model was established by highfat diet(HFD)feeding combined with intraperitoneal injection of streptozotocin(STZ).Thirty-six C57BL/6N male mice were randomly divided into six groups(n=6 each).All groups were orally administered with distilled water(control and model),dapagliflozin or CDPs for 4 weeks.Changes in physiological indices,renal function,inflammatory factors and the intestinal microbiota were assessed.The results showed that CDPs significantly improved the general condition and attenuated the renal histopathological changes,and reduced the levels of blood glucose,urinary protein and inflammatory factors in DN mice.Additionally,CDPs affected the balance of intestinal microbiota,increased the abundance of beneficial bacteria and decreased potential pathogenic bacteria,which in turn improved intestinal barrier function.CDPs also inhibited the activation of the Toll-like receptor 4/nuclear factor-κB(TLR4/NF-κB)signaling pathway and reduced the release of lipopolysaccharide(LPS).In conclusion,CDPs exhibit an ameliorative effect on DN in mice by affecting the intestinal microbiota and inhibiting inflammatory signaling pathways.This finding offers new insights into the treatment of DN.