{"title":"水蛭素通过诱导自噬抑制NLRP3炎性体激活减轻肾纤维化。","authors":"Chunli Long, Fang Lan, Hui Xie, Jiefang Chen, Yongxiang Xie","doi":"10.1093/bbb/zbaf114","DOIUrl":null,"url":null,"abstract":"<p><p>Renal fibrosis is a pathological feature of chronic kidney injury that contributes to renal failure. This study aimed to explore the effect of Hirudin on renal fibrosis. The anti-fibrotic effect of Hirudin was evaluated using unilateral ureteral obstruction (UUO) rats and TGF-β-treated HK-2 cells. The autophagy inhibitor 3-Methyladenine was used to further explore the potential mechanism. Hirudin treatment significantly reduced UUO-induced elevations in blood urea nitrogen, creatinine, and alpha-smooth muscle actin (α-SMA) levels, and improved kidney injury and renal fibrosis. In addition, Hirudin markedly decreased NLRP3 inflammasome-related protein expression and increased autophagy-related protein expression in the kidneys of UUO rats. Hirudin significantly increased cell viability, reduced α-SMA and NLRP3 inflammasome-related protein levels, and increased autophagy-related protein levels in TGF-β-treated HK-2 cells. However, the effects of Hirudin were counteracted by 3-Methyladenine. In conclusion, Hirudin inhibits the activation of NLRP3 inflammasome by inducing autophagy to improve renal fibrosis.</p>","PeriodicalId":9175,"journal":{"name":"Bioscience, Biotechnology, and Biochemistry","volume":" ","pages":""},"PeriodicalIF":1.3000,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Hirudin Alleviates Renal Fibrosis by Inducing Autophagy to Suppress NLRP3 Inflammasome Activation.\",\"authors\":\"Chunli Long, Fang Lan, Hui Xie, Jiefang Chen, Yongxiang Xie\",\"doi\":\"10.1093/bbb/zbaf114\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Renal fibrosis is a pathological feature of chronic kidney injury that contributes to renal failure. This study aimed to explore the effect of Hirudin on renal fibrosis. The anti-fibrotic effect of Hirudin was evaluated using unilateral ureteral obstruction (UUO) rats and TGF-β-treated HK-2 cells. The autophagy inhibitor 3-Methyladenine was used to further explore the potential mechanism. Hirudin treatment significantly reduced UUO-induced elevations in blood urea nitrogen, creatinine, and alpha-smooth muscle actin (α-SMA) levels, and improved kidney injury and renal fibrosis. In addition, Hirudin markedly decreased NLRP3 inflammasome-related protein expression and increased autophagy-related protein expression in the kidneys of UUO rats. Hirudin significantly increased cell viability, reduced α-SMA and NLRP3 inflammasome-related protein levels, and increased autophagy-related protein levels in TGF-β-treated HK-2 cells. However, the effects of Hirudin were counteracted by 3-Methyladenine. In conclusion, Hirudin inhibits the activation of NLRP3 inflammasome by inducing autophagy to improve renal fibrosis.</p>\",\"PeriodicalId\":9175,\"journal\":{\"name\":\"Bioscience, Biotechnology, and Biochemistry\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2025-07-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Bioscience, Biotechnology, and Biochemistry\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.1093/bbb/zbaf114\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bioscience, Biotechnology, and Biochemistry","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1093/bbb/zbaf114","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Hirudin Alleviates Renal Fibrosis by Inducing Autophagy to Suppress NLRP3 Inflammasome Activation.
Renal fibrosis is a pathological feature of chronic kidney injury that contributes to renal failure. This study aimed to explore the effect of Hirudin on renal fibrosis. The anti-fibrotic effect of Hirudin was evaluated using unilateral ureteral obstruction (UUO) rats and TGF-β-treated HK-2 cells. The autophagy inhibitor 3-Methyladenine was used to further explore the potential mechanism. Hirudin treatment significantly reduced UUO-induced elevations in blood urea nitrogen, creatinine, and alpha-smooth muscle actin (α-SMA) levels, and improved kidney injury and renal fibrosis. In addition, Hirudin markedly decreased NLRP3 inflammasome-related protein expression and increased autophagy-related protein expression in the kidneys of UUO rats. Hirudin significantly increased cell viability, reduced α-SMA and NLRP3 inflammasome-related protein levels, and increased autophagy-related protein levels in TGF-β-treated HK-2 cells. However, the effects of Hirudin were counteracted by 3-Methyladenine. In conclusion, Hirudin inhibits the activation of NLRP3 inflammasome by inducing autophagy to improve renal fibrosis.
期刊介绍：
Bioscience, Biotechnology, and Biochemistry publishes high-quality papers providing chemical and biological analyses of vital phenomena exhibited by animals, plants, and microorganisms, the chemical structures and functions of their products, and related matters. The Journal plays a major role in communicating to a global audience outstanding basic and applied research in all fields subsumed by the Japan Society for Bioscience, Biotechnology, and Agrochemistry (JSBBA).
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