摘要
高尿酸血症是由于体内嘌呤代谢紊乱而引起的代谢性疾病,主要表现为血清尿酸浓度增高,发病机制与体内尿酸生成过多和(或)尿酸排泄减少密切相关。体内尿酸代谢受多种基因和蛋白的调控,相关基因碱基的突变或缺失可导致其编码的的尿酸转运蛋白功能障碍,血清尿酸浓度异常增高从而引发高尿酸血症。临床治疗高尿酸血症的药物多通过调控尿酸转运的相关基因和蛋白的表达而发挥作用,笔者以此为出发点,总结治疗药物的相关作用靶点及其降低体内尿酸水平的作用机制,为新药的研发提供参考依据。
Hyperuricemia is a metabolic disease resulting from purine metabolic disturbance in the body, its main clinical manifestations are the increase of serum uric acid concentration, and its pathogenesis is closely related to the excessive production of uric acid and the decrease of uric acid excretion. The metabolism of uric acid in the body is regulated by many genes and proteins, mutation or deletion of the related gene base can lead to the dysfunction of the encode uric acid transporter, and the abnormal increase in serum uric acid concentration can cause hyperuricemia. The drugs used to treat hyperuricemia can play an important role in regulating the expression of related genes and proteins of transport of uric acid. In this paper, the author take this as a starting point, summarized the related action targets and mechanism of lowering uric acid level in vivo of therapeutic drugs to provide reference for the research and development of new drugs.
作者
李萍
宋志斌
陈苗苗
宋娟
崔红霞
LI Ping;SONG Zhi-bin;CHEN Miao-miao;SONG Juan;CUI Hong-xia(Pharmacy School,Qiqihar Medical University,Heilongjiang Province,Qiqihar 161006,China)
出处
《中国当代医药》
2018年第21期16-19,共4页
China Modern Medicine
基金
黑龙江省大学生创新创业训练计划项目(201611230025)