{"title":"尾状连翘（拇指）直流。提取物通过调节TGF-β1通路和尿酸转运蛋白减轻高尿酸血症诱导的肾纤维化：来自体外和体内研究的证据","authors":"Hui-Hsuan Lin , Yu-Hsuan Liang , Charng-Cherng Chyau , Chiao-Yun Tseng , Jun-Quan Zhang , Jing-Hsien Chen","doi":"10.1016/j.jep.2025.119609","DOIUrl":null,"url":null,"abstract":"<div><h3>Ethnopharmacological relevance</h3><div><em>Desmodium caudatum</em> (Thunb.) DC., a traditional Chinese medicinal herb, has been used to treat conditions such as rheumatic back pain, diarrhea, jaundice-related hepatitis, and abscesses; it also serves as an anthelmintic. The extract of <em>Desmodium caudatum</em> (Thunb.) DC. (DCE) is also known for its antioxidant and anti-inflammatory properties. However, its impact on kidney fibrosis remains unclear.</div></div><div><h3>Aim of the study</h3><div>This study investigated whether DCE can alleviate hyperuricemia-induced kidney fibrosis by modulating the transforming growth factor-β1 (TGF-β1) pathway, activating epithelial-mesenchymal transition (EMT), and regulating uric acid transporters.</div></div><div><h3>Materials and methods</h3><div>NRK52E cells were exposed to uric acid (UA) followed by DCE and isovitexin (IV) for 24 h. Cell damage was assessed using an Oxidative Stress Kit, ELISA, Gelatin Zymography, and Western blotting. In parallel, adenine-induced C57BL/6 mice received DCE and IV treatment for 11 weeks. After sacrifice, renal injury was assessed through histopathological examination and protein expression analysis of fibrosis markers, EMT indicators, and uric acid transporters.</div></div><div><h3>Results</h3><div>DCE reduced reactive oxygen species (ROS) accumulation in uric acid-induced NRK52E cells and inhibited EMT by suppressing TGF-β1 and Slug while restoring E-cadherin expression. DCE treatment reduced fibrosis-related proteins (CTGF, collagen I, fibronectin, and α-SMA) in UA-treated cells and modulated uric acid transporters by increasing ABCG2 and OAT3 while decreasing URAT1 and GLUT9. In adenine-induced hyperuricemic C57BL/6 mice, DCE administration reduced serum uric acid levels and xanthine oxidase activity. Histological analysis showed that DCE attenuated renal fibrosis through decreased glomerular atrophy, reduced collagen deposition, and diminished α-SMA and fibronectin expression.</div></div><div><h3>Conclusion</h3><div>Our study demonstrates that DCE exerts protective benefits against hyperuricemia-induced renal fibrosis. The potential mechanism may involve suppressing the TGF-β1 signaling pathway and regulating the uric acid transporter, thereby mitigating kidney injury.</div></div>","PeriodicalId":15761,"journal":{"name":"Journal of ethnopharmacology","volume":"345 ","pages":"Article 119609"},"PeriodicalIF":5.4000,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Desmodium caudatum (Thunb.) DC. extract attenuates hyperuricemia-induced renal fibrosis via modulating TGF-β1 pathway and uric acid transporters: Evidence from in vitro and in vivo studies\",\"authors\":\"Hui-Hsuan Lin , Yu-Hsuan Liang , Charng-Cherng Chyau , Chiao-Yun Tseng , Jun-Quan Zhang , Jing-Hsien Chen\",\"doi\":\"10.1016/j.jep.2025.119609\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Ethnopharmacological relevance</h3><div><em>Desmodium caudatum</em> (Thunb.) DC., a traditional Chinese medicinal herb, has been used to treat conditions such as rheumatic back pain, diarrhea, jaundice-related hepatitis, and abscesses; it also serves as an anthelmintic. The extract of <em>Desmodium caudatum</em> (Thunb.) DC. (DCE) is also known for its antioxidant and anti-inflammatory properties. However, its impact on kidney fibrosis remains unclear.</div></div><div><h3>Aim of the study</h3><div>This study investigated whether DCE can alleviate hyperuricemia-induced kidney fibrosis by modulating the transforming growth factor-β1 (TGF-β1) pathway, activating epithelial-mesenchymal transition (EMT), and regulating uric acid transporters.</div></div><div><h3>Materials and methods</h3><div>NRK52E cells were exposed to uric acid (UA) followed by DCE and isovitexin (IV) for 24 h. Cell damage was assessed using an Oxidative Stress Kit, ELISA, Gelatin Zymography, and Western blotting. In parallel, adenine-induced C57BL/6 mice received DCE and IV treatment for 11 weeks. After sacrifice, renal injury was assessed through histopathological examination and protein expression analysis of fibrosis markers, EMT indicators, and uric acid transporters.</div></div><div><h3>Results</h3><div>DCE reduced reactive oxygen species (ROS) accumulation in uric acid-induced NRK52E cells and inhibited EMT by suppressing TGF-β1 and Slug while restoring E-cadherin expression. DCE treatment reduced fibrosis-related proteins (CTGF, collagen I, fibronectin, and α-SMA) in UA-treated cells and modulated uric acid transporters by increasing ABCG2 and OAT3 while decreasing URAT1 and GLUT9. In adenine-induced hyperuricemic C57BL/6 mice, DCE administration reduced serum uric acid levels and xanthine oxidase activity. Histological analysis showed that DCE attenuated renal fibrosis through decreased glomerular atrophy, reduced collagen deposition, and diminished α-SMA and fibronectin expression.</div></div><div><h3>Conclusion</h3><div>Our study demonstrates that DCE exerts protective benefits against hyperuricemia-induced renal fibrosis. The potential mechanism may involve suppressing the TGF-β1 signaling pathway and regulating the uric acid transporter, thereby mitigating kidney injury.</div></div>\",\"PeriodicalId\":15761,\"journal\":{\"name\":\"Journal of ethnopharmacology\",\"volume\":\"345 \",\"pages\":\"Article 119609\"},\"PeriodicalIF\":5.4000,\"publicationDate\":\"2025-04-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of ethnopharmacology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0378874125002934\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/3/8 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"CHEMISTRY, MEDICINAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of ethnopharmacology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0378874125002934","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/3/8 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"CHEMISTRY, MEDICINAL","Score":null,"Total":0}
Desmodium caudatum (Thunb.) DC. extract attenuates hyperuricemia-induced renal fibrosis via modulating TGF-β1 pathway and uric acid transporters: Evidence from in vitro and in vivo studies
Ethnopharmacological relevance
Desmodium caudatum (Thunb.) DC., a traditional Chinese medicinal herb, has been used to treat conditions such as rheumatic back pain, diarrhea, jaundice-related hepatitis, and abscesses; it also serves as an anthelmintic. The extract of Desmodium caudatum (Thunb.) DC. (DCE) is also known for its antioxidant and anti-inflammatory properties. However, its impact on kidney fibrosis remains unclear.
Aim of the study
This study investigated whether DCE can alleviate hyperuricemia-induced kidney fibrosis by modulating the transforming growth factor-β1 (TGF-β1) pathway, activating epithelial-mesenchymal transition (EMT), and regulating uric acid transporters.
Materials and methods
NRK52E cells were exposed to uric acid (UA) followed by DCE and isovitexin (IV) for 24 h. Cell damage was assessed using an Oxidative Stress Kit, ELISA, Gelatin Zymography, and Western blotting. In parallel, adenine-induced C57BL/6 mice received DCE and IV treatment for 11 weeks. After sacrifice, renal injury was assessed through histopathological examination and protein expression analysis of fibrosis markers, EMT indicators, and uric acid transporters.
Results
DCE reduced reactive oxygen species (ROS) accumulation in uric acid-induced NRK52E cells and inhibited EMT by suppressing TGF-β1 and Slug while restoring E-cadherin expression. DCE treatment reduced fibrosis-related proteins (CTGF, collagen I, fibronectin, and α-SMA) in UA-treated cells and modulated uric acid transporters by increasing ABCG2 and OAT3 while decreasing URAT1 and GLUT9. In adenine-induced hyperuricemic C57BL/6 mice, DCE administration reduced serum uric acid levels and xanthine oxidase activity. Histological analysis showed that DCE attenuated renal fibrosis through decreased glomerular atrophy, reduced collagen deposition, and diminished α-SMA and fibronectin expression.
Conclusion
Our study demonstrates that DCE exerts protective benefits against hyperuricemia-induced renal fibrosis. The potential mechanism may involve suppressing the TGF-β1 signaling pathway and regulating the uric acid transporter, thereby mitigating kidney injury.
期刊介绍：
The Journal of Ethnopharmacology is dedicated to the exchange of information and understandings about people''s use of plants, fungi, animals, microorganisms and minerals and their biological and pharmacological effects based on the principles established through international conventions. Early people confronted with illness and disease, discovered a wealth of useful therapeutic agents in the plant and animal kingdoms. The empirical knowledge of these medicinal substances and their toxic potential was passed on by oral tradition and sometimes recorded in herbals and other texts on materia medica. Many valuable drugs of today (e.g., atropine, ephedrine, tubocurarine, digoxin, reserpine) came into use through the study of indigenous remedies. Chemists continue to use plant-derived drugs (e.g., morphine, taxol, physostigmine, quinidine, emetine) as prototypes in their attempts to develop more effective and less toxic medicinals.
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