高尿酸血症
肠道菌群
尿酸
排泄
内科学
医学
生物
生物化学
作者
Yang Wang,Jing Xie,Siya Yan,Mei‐Fang Cheng,Jing Yan,Ke Li,Fengyan Yang,Jiandong Li,Qian Chen,Yuzheng Wu,Yi Zhang,Dan Wang,Tao Wang
标识
DOI:10.1097/hm9.0000000000000156
摘要
Objective: Hyperuricemia (HUA) is a metabolic disease that threatens human health. The role of Penthorum chinense Pursh. (PCP) in the treatment of HUA has begun to receive attention in recent years. This study aimed to investigate the effects and potential mechanisms of PCP in HUA treatment. Methods: A HUA murine model was induced in C57/BL6 mice using potassium oxonate (PO) and adenine (AD). Serum uric acid (SUA) was measured using ultra-performance liquid chromatography (UPLC). Serum creatinine (Scr) was detected using a creatine oxidase assay kit, and serum blood urea nitrogen (BUN) was detected using a urease indophenol blue assay kit. Protein expression levels were detected using western blotting, and gut microbiota were detected using 16S rRNA. Results: PCP substantially improved the serum contents of SUA, Scr, and BUN and alleviated kidney injury. PCP promotes renal uric acid excretion by downregulating GLUT9 and URAT1 expression and upregulating ABCG2 and OAT1 expression PCP also regulated the NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) pathway and reduced the expression of inflammatory factors, thus attenuating kidney injury in HUA mice. PCP regulated the structure of the gut microbiota, including the relative abundance of beneficial bacteria, such as Lactobacillus and Alistipes, which promoted uric acid metabolism and anti-inflammatory effects. Conclusions: PCP can reduce uric acid levels by promoting renal uric acid excretion and regulating the gut microbiota. PCP improves kidney injury by inhibiting the activation of the NLRP3 signaling pathway and reducing the levels of inflammatory factors.
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