Taurine decreased uric acid levels in hyperuricemic rats and alleviated kidney injury

被引:44
作者
Feng, Ying [1 ]
Sun, Fang [2 ]
Gao, Yongchao [1 ]
Yang, Jiancheng [1 ]
Wu, Gaofeng [1 ]
Lin, Shumei [1 ]
Hu, Jianmin [1 ]
机构
[1] Shenyang Agr Univ, Coll Anim Sci & Vet Med, Key Lab Zoonosis Liaoning Prov, Shenyang 110866, Peoples R China
[2] China Japan Friendship Hosp, Dept Pediat, 2 Yinghua Dongjie, Beijing 100029, Peoples R China
基金
中国国家自然科学基金;
关键词
Taurine; Uric acid; Hyperuricemia; Kidney injury; RENAL-DISEASE; HYPERTENSION; EXPRESSION; TRANSPORT; MORTALITY; GOUT;
D O I
10.1016/j.bbrc.2017.05.139
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Hyperuricemia can lead to direct kidney damage. Taurine participates in several renal physiological processes and has been shown as a renoprotective agent. It has been reported that taurine could reduce uric acid levels in diabetic rats, but to date there was no research on the effects of taurine on hyperuricemic rats with kidney injury. In present study, hyperuricemic rat models were induced by intragastric administration of adenine and ethambutol hydrochloride for 10 days, and taurine (1% or 2%) were added in the drinking water 7 days in advance for consecutively 17 days. The results showed that taurine alleviated renal morphological and pathological changes as well as kidney dysfunction in hyperuricemic rats. Taurine could efficiently decrease the elevated xanthine oxidase activities in hyperuricemic rats, indicating its effect on the regulation of uric acid formation. The reabsorption and secretion of uric acid are dependent on a number of urate transporters. Expressions of three urate transporters were significantly down-regulated in hyperuricemic rats, while taurine prevented the decrease of mRNA and protein expression levels of these urate transporters. The results indicate that taurine might play a role in the regulation of renal uric acid excretion. Therefore, taurine could be a promising agent for the treatment of hyperuricemia. (C) 2017 Elsevier Inc. All rights reserved.
引用
收藏
页码:312 / 318
页数:7
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