NLRP3及其抑制药物在肾缺血/再灌注损伤中的研究进展  

Research progress of NLRP3 and its inhibitors in renal ischemia-reperfusion injury

作　　者：陈涛 蔡飞[3] 江波涛[4] CHEN Tao;CAI Fei;JIANG Bo-tao(School of Pharmacy,Hubei University of Science and Technology,Xianning Hubei 437100,China;Dept of Pharmacy,Xianning Central Hospital/The First Affiliated Hospital of Hubei University of Science and Technology,Xianning Hubei 437100,China;Hubei Key Laboratory of Diabetes and Angiopathy,Hubei University of Science and Technology,Xianning Hubei 437100,China;Dept of Urology,Xianning Central Hospital/The First Affiliated Hospital of Hubei University of Science and Technology,Xianning Hubei 437100,China)

机构地区：[1]湖北科技学院药学院 [2]咸宁市中心医院/湖北科技学院附属第一医院药学部 [3]湖北科技学院糖尿病心脑血管病变湖北省重点实验室 [4]咸宁市中心医院/湖北科技学院附属第一医院泌尿外科,湖北咸宁437100

出　　处：《中国药理学通报》2022年第1期22-25,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 81870576);湖北省卫健委资助项目(WJ 2021M091);湖北省高校优秀中青年科技创新团队项目(No T201921)。

摘　　要：Nod样受体蛋白3(Nod-1ike receptor protein 3,NLRP3)是肾脏中最具代表性的炎症小体,在肾缺血/再灌注损伤(renal-ischemic reperfusion injury, RIRI)的进程中,NLRP3可通过炎症小体依赖途径和非炎症小体依赖途径介导疾病发生,并且在被多种途径激活后可导致损伤进一步加重;多项研究表明,多种药物或化合物可通过抑制NLRP3激活来减轻RIRI。因此,研究RIRI中NLRP3的致病机制、激活途径以及抑制药物或化合物至关重要,该文将对以上研究的最新进展进行综述。Nod-like receptor protein 3(NLRP3) is the most representative inflammasome in the kidney, which can mediate the occurrence of diseases through inflammasome dependent and non inflammasome dependent pathways in the process of renal ischemia-reperfusion injury(RIRI). After being activated by many ways, the damage will be further aggravated. Studies have shown that many drugs or compounds can reduce RIRI by inhibiting the activation of NLRP3.Therefore, it is very important to study the pathogenesis, activation pathway and inhibitors or compounds of NLRP3 in RIRI. This article will review the latest progress of the above research.

关 键 词：NLRP3 肾脏 缺血/再灌注损伤 活性氧 药物 化合物 

分 类 号：R322.61[医药卫生—人体解剖和组织胚胎学] R364.12[医药卫生—基础医学]