{"title":"microRNA-216a-5p 通过抑制 FASL 的表达减轻小鼠急性肾损伤。","authors":"Biying Zhou, Ruirui Luo, Yanlin Sun, Aixiang Yang","doi":"10.1159/000539980","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The aim of this present work was to investigate the mechanism of the microRNA (miR)-216a-5p/FASL axis in mice with acute kidney injury (AKI).</p><p><strong>Methods: </strong>Mice kidney ischemia/reperfusion (I/R) injury was used as AKI models in this study. I/R mice were injected with miR-216a-5p- and FASL-related constructs to investigate potential mechanisms of kidney protection. Kidney function, inflammation, oxidative stress, and kidney cell apoptosis were assessed after 24 h of reperfusion. In vitro, the hypoxia-reoxygenation (H/R) model was used with kidney tubular epithelial cells (TECs) to mimic kidney I/R injury. H/R-treated TECs were transfected with miR-216a-5p- and FASL-related constructs to detect cell viability, inflammation, and oxidative stress. MiR-216a-5p and FASL expression levels in mouse kidney tissues and in H/R-treated TECs were detected.</p><p><strong>Results: </strong>MiR-216a-5p was downregulated and FASL was upregulated in kidney tissues of I/R mice and H/R-treated TECs. Upregulating miR-216a-5p attenuated kidney cell apoptosis and the damage of kidney function, and reduced inflammatory factor levels and oxidative stress response in kidney tissues of I/R mice. Upregulating miR-216a-5p advanced cell viability and reduced inflammatory factor levels and oxidative stress response in H/R-treated TECs. Downregulation of FASL effectively reversed the influences of downregulation of miR-216a-5p on kidney injury in mice and kidney TEC survival.</p><p><strong>Conclusion: </strong>Our study reveals that miR-216a-5p reduces I/R-induced pathological kidney damage in AKI via suppressing FASL.</p>","PeriodicalId":12222,"journal":{"name":"European Surgical Research","volume":null,"pages":null},"PeriodicalIF":1.7000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"MicroRNA-216a-5p Alleviates Acute Kidney Injury of Mice via Suppressing FAS Ligand Expression.\",\"authors\":\"Biying Zhou, Ruirui Luo, Yanlin Sun, Aixiang Yang\",\"doi\":\"10.1159/000539980\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>The aim of this present work was to investigate the mechanism of the microRNA (miR)-216a-5p/FASL axis in mice with acute kidney injury (AKI).</p><p><strong>Methods: </strong>Mice kidney ischemia/reperfusion (I/R) injury was used as AKI models in this study. I/R mice were injected with miR-216a-5p- and FASL-related constructs to investigate potential mechanisms of kidney protection. Kidney function, inflammation, oxidative stress, and kidney cell apoptosis were assessed after 24 h of reperfusion. In vitro, the hypoxia-reoxygenation (H/R) model was used with kidney tubular epithelial cells (TECs) to mimic kidney I/R injury. H/R-treated TECs were transfected with miR-216a-5p- and FASL-related constructs to detect cell viability, inflammation, and oxidative stress. MiR-216a-5p and FASL expression levels in mouse kidney tissues and in H/R-treated TECs were detected.</p><p><strong>Results: </strong>MiR-216a-5p was downregulated and FASL was upregulated in kidney tissues of I/R mice and H/R-treated TECs. Upregulating miR-216a-5p attenuated kidney cell apoptosis and the damage of kidney function, and reduced inflammatory factor levels and oxidative stress response in kidney tissues of I/R mice. Upregulating miR-216a-5p advanced cell viability and reduced inflammatory factor levels and oxidative stress response in H/R-treated TECs. Downregulation of FASL effectively reversed the influences of downregulation of miR-216a-5p on kidney injury in mice and kidney TEC survival.</p><p><strong>Conclusion: </strong>Our study reveals that miR-216a-5p reduces I/R-induced pathological kidney damage in AKI via suppressing FASL.</p>\",\"PeriodicalId\":12222,\"journal\":{\"name\":\"European Surgical Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"European Surgical Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1159/000539980\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/8/2 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"SURGERY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Surgical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000539980","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/2 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"SURGERY","Score":null,"Total":0}
引用次数: 0
摘要
引言本研究旨在探讨急性肾损伤（AKI）小鼠体内microRNA（miR）-216a-5p/FASL轴的作用机制：方法：本研究以小鼠肾脏缺血再灌注（I/R）损伤为 AKI 模型。再灌注 24 小时后评估肾功能、炎症、氧化应激和肾细胞凋亡。在体外，利用肾小管上皮细胞（TECs）的低氧-复氧（H/R）模型模拟肾脏I/R损伤。结果：在I/R小鼠肾组织和H/R处理的TECs中，miR-216a-5p下调，FASL上调。上调 miR-216a-5p 可减轻 I/R 小鼠肾脏组织中肾细胞凋亡和肾功能损伤，降低炎症因子水平和氧化应激反应。上调miR-216a-5p可提高H/R处理的TECs细胞活力，降低炎症因子水平和氧化应激反应。下调FASL可有效逆转下调miR-216a-5p对小鼠肾损伤和肾脏TEC存活的影响：我们的研究发现，miR-216a-5p可通过抑制FASL减轻I/R诱导的AKI病理肾损伤。
MicroRNA-216a-5p Alleviates Acute Kidney Injury of Mice via Suppressing FAS Ligand Expression.
Introduction: The aim of this present work was to investigate the mechanism of the microRNA (miR)-216a-5p/FASL axis in mice with acute kidney injury (AKI).
Methods: Mice kidney ischemia/reperfusion (I/R) injury was used as AKI models in this study. I/R mice were injected with miR-216a-5p- and FASL-related constructs to investigate potential mechanisms of kidney protection. Kidney function, inflammation, oxidative stress, and kidney cell apoptosis were assessed after 24 h of reperfusion. In vitro, the hypoxia-reoxygenation (H/R) model was used with kidney tubular epithelial cells (TECs) to mimic kidney I/R injury. H/R-treated TECs were transfected with miR-216a-5p- and FASL-related constructs to detect cell viability, inflammation, and oxidative stress. MiR-216a-5p and FASL expression levels in mouse kidney tissues and in H/R-treated TECs were detected.
Results: MiR-216a-5p was downregulated and FASL was upregulated in kidney tissues of I/R mice and H/R-treated TECs. Upregulating miR-216a-5p attenuated kidney cell apoptosis and the damage of kidney function, and reduced inflammatory factor levels and oxidative stress response in kidney tissues of I/R mice. Upregulating miR-216a-5p advanced cell viability and reduced inflammatory factor levels and oxidative stress response in H/R-treated TECs. Downregulation of FASL effectively reversed the influences of downregulation of miR-216a-5p on kidney injury in mice and kidney TEC survival.
Conclusion: Our study reveals that miR-216a-5p reduces I/R-induced pathological kidney damage in AKI via suppressing FASL.
期刊介绍：
''European Surgical Research'' features original clinical and experimental papers, condensed reviews of new knowledge relevant to surgical research, and short technical notes serving the information needs of investigators in various fields of operative medicine. Coverage includes surgery, surgical pathophysiology, drug usage, and new surgical techniques. Special consideration is given to information on the use of animal models, physiological and biological methods as well as biophysical measuring and recording systems. The journal is of particular value for workers interested in pathophysiologic concepts, new techniques and in how these can be introduced into clinical work or applied when critical decisions are made concerning the use of new procedures or drugs.
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