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作 者:赖灿 李乐乐 胡塔拉 孟彦 LAI Can;LI Lele;HU Tala;MENG Yan(Graduate School of Inner Mongolia Medical University,Hohhot 010110,China;Division of Nephrology,the Affiliated Hospital of Inner Mongolia Medical University,Hohhot 010050,China)
机构地区:[1]内蒙古医科大学研究生院,呼和浩特010110 [2]内蒙古医科大学附属医院肾内科,呼和浩特010050
出 处:《实验动物与比较医学》2023年第2期163-172,共10页Laboratory Animal and Comparative Medicine
基 金:国家自然科学基金资助项目“组蛋白去乙酰化酶Sirt6通过Wnt/β-Catenin信号通路对慢性肾脏病肾性骨病的控制作用及机制研究”(81960143);内蒙古自治区自然科学基金项目“RNA m6A甲基化在慢性肾脏病肾小管间质纤维化中的作用及机制研究”(2022MS08063);内蒙古医科大学“致远”人才计划-“治学”人才项目(ZY0130015)。
摘 要:肾脏间质纤维化是许多肾脏疾病不断进展的共同路径。不管是各种慢性肾脏病,或是各种因素所引起的无法完全恢复的急性肾损伤,其进展过程多数是在经过肾脏间质纤维化后进入终末期肾功能衰竭。肾脏间质纤维化的动物模型是探索肾脏间质纤维化发生机制和新诊断治疗方法的主要研究工具。不同的动物模型各有特色,研究者可依据个人经验及实验目的建立不同的模型,并以此为基础开展科学研究,为肾脏疾病的防治提供更多新方法、新思路。本文着重综合阐述目前常见的几种肾脏间质纤维化动物模型,包括单侧输尿管梗阻、缺血-再灌注损伤、肾大部切除、微栓塞诱导形成的手术模型,环孢素A、阿霉素、马兜铃酸、氯化汞、庆大霉素、马兜铃酸、顺铂、腺嘌呤诱导形成的化学模型,转基因杂交、肾损伤因子-1诱导形成的转基因修饰模型,双侧缺血-再灌注损伤术联合庆大霉素、单侧肾切除联合血管紧张素Ⅱ、单侧缺血-再灌注损伤术联合pLVX-shTNC质粒诱导形成的复合模型,以供相关研究人员了解和借鉴。Renal interstitial fibrosis is a common pathway in the progression of many renal diseases.Whether it is chronic kidney disease or acute kidney injury that cannot be fully recovered,the progression process mostly enters end-stage renal failure after renal interstitial fibrosis.The animal model of renal interstitial fibrosis is an important research tool for exploring the pathogenesis of renal interstitial fibrosis and new diagnostic and treatment methods.Different animal models have their own characteristics.Researchers can establish different models based on their own experience and experimental purposes,and carry out scientific research on this basis to provide more new methods for the prevention and treatment of kidney diseases.The authors focused on several common animal models of renal interstitial fibrosis to provide the reference for related researchers,including surgical models induced by unilateral ureteral obstruction,ischemia-reperfusion injury,5/6 nephrectomy,and microembolization;chemical models induced by cyclosporine A,adriamycin,aristolochic acid,mercuric chloride(HgCl2),gentamicin,cisplatin,and adenine;transgenic hybridization and kidney injury molecule 1(KIM-1)induced transgenic modification model;composite model induced by bilateral ischemia-reperfusion injury(BIRI)combined with gentamicin,unilateral nephrectomy combined with angiotensin II(Ang II),and unilateral ischemia-reperfusion injury(UIRI)combined with pLVX-shTNC plasmid.
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