Chen Wu-Jin, Wang Jian-Ping, Zhou Jing-Ru, He Yi, An Dong-Qing, Tian Ting-Ting, Liang Mei-Ting, Aikepa Dilinuer, Kahaer Mayina, Sun Yu-Ping
Department of Morphology, School of Basic Medical Sciences, Institute of Medical Sciences of Xinjiang Medical University, Xinjiang Medical University, Urumqi, 830017, Xinjiang, China; Key Laboratory of Xinjiang Uygur Autonomous Region, Laboratory of Molecular Biology of Endemic Diseases, Urumqi, 830017, Xinjiang, China.
Xinjiang Laboratory of Famous Prescription and Science of Formulas, Urumqi, 830002, Xinjiang, China; Department of Cardiology, The Fourth Affiliated Hospital of Xinjiang Medical University, Urumqi, 830002, Xinjiang, China.
Microb Pathog. 2025 Oct;207:107922. doi: 10.1016/j.micpath.2025.107922. Epub 2025 Jul 21.
The compound Bai Mao Yin (BMY) has demonstrated therapeutic efficacy in reducing uric acid (UA) levels; however, its underlying mechanisms remain unclear.
The UA-lowering effects of BMY were evaluated in a cohort of 40 patients with hyperuricemia (HUA) who received BMY treatment for 90 days. Fecal samples were collected at baseline (day 0), mid-treatment (day 30), and post-treatment (day 90) for metagenomic sequencing to analyze changes in gut microbiota and identify potential BMY targets in HUA. These clinical findings were validated in a hyperuricemic mouse model induced by xanthine and potassium oxonate. Mouse fecal samples were analyzed via 16S rDNA (V3-V4 region) sequencing to assess microbiota shifts. Additionally, fecal microbiota transplantation (FMT) from BMY-treated mice to HUA mice and in vitro cell experiments using HK2 cells were conducted to investigate the roles of BMY and the reconstructed microbiota in UA metabolism, renal UA transport, and inflammation through upstream signaling pathways.
Clinical cohort studies demonstrated that the BMY effectively lowers UA levels in patients with HUA without inducing hepatorenal toxicity. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis of metagenomic data revealed that BMY modulates the gut microbiota and influences ATP-binding cassette transporters and UA metabolism-related pathways. In animal models, BMY increased the relative abundance of beneficial gut bacteria, reduced intestinal permeability, and regulated UA transporters in both intestinal and renal systems, contributing to UA reduction. In vitro assays showed that BMY directly decreased UA levels in the cell supernatant and suppressed interleukin-1β (IL-1β) and interleukin-6 (IL-6) expression by downregulating the TLR4/MYD88/NFκB signaling pathway, thereby alleviating inflammation.
Compound BMY was found to improve the intestinal microenvironment and modulate UA transport via the enterorenal axis, effectively reducing HUA.
复方白毛银（BMY）已显示出降低尿酸（UA）水平的治疗效果；然而，其潜在机制仍不清楚。
对40例高尿酸血症（HUA）患者进行队列研究，给予BMY治疗90天，评估其降尿酸效果。在基线（第0天）、治疗中期（第30天）和治疗后（第90天）采集粪便样本进行宏基因组测序，分析肠道微生物群的变化，并确定HUA中潜在的BMY作用靶点。这些临床发现在由黄嘌呤和氧嗪酸钾诱导的高尿酸血症小鼠模型中得到验证。通过16S rDNA（V3-V4区域）测序分析小鼠粪便样本，以评估微生物群的变化。此外，进行了从BMY处理的小鼠到HUA小鼠的粪便微生物群移植（FMT）以及使用HK2细胞的体外细胞实验，以研究BMY和重建的微生物群在UA代谢、肾脏UA转运以及通过上游信号通路介导的炎症中的作用。
临床队列研究表明，BMY能有效降低HUA患者的UA水平，且不引起肝肾毒性。对宏基因组数据的京都基因与基因组百科全书（KEGG）富集分析表明，BMY可调节肠道微生物群，并影响ATP结合盒转运蛋白和UA代谢相关途径。在动物模型中，BMY增加了有益肠道细菌的相对丰度，降低了肠道通透性，并调节了肠道和肾脏系统中的UA转运蛋白，从而有助于降低UA水平。体外实验表明，BMY可直接降低细胞上清液中的UA水平，并通过下调TLR4/MYD88/NFκB信号通路抑制白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）的表达，从而减轻炎症。
发现复方BMY可改善肠道微环境，并通过肠肾轴调节UA转运，有效降低HUA。
