文献类型：期刊文献

英文题名：Hypouricemic, hepatoprotective and nephroprotective roles of oligopeptides derived from Auxis thazard protein in hyperuricemic mice

作者：Wei, Liuyi[1];Ji, Hongwu[1,2,3,4,5];Song, Wenkui[1];Peng, Shuo[1];Zhan, Suhong[1];Qu, Yushan[1];Chen, Ming[1];Zhang, Di[1];Liu, Shucheng[1,2,3,4,5,6,7]

机构：[1]Guangdong Ocean Univ, Coll Food Sci & Technol, Zhanjiang 524088, Peoples R China;[2]Guangdong Prov Key Lab Aquat Prod Proc & Safety, Zhanjiang 524088, Peoples R China;[3]Guangdong Prov Engn Lab Marine Biol Prod, Zhanjiang 524088, Peoples R China;[4]Guangdong Prov Engn Technol Res Ctr Marine Food, Zhanjiang 524088, Peoples R China;[5]Key Lab Adv Proc Aquat Prod Guangdong Higher Educ, Zhanjiang 524088, Peoples R China;[6]Collaborat Innovat Ctr Seafood Deep Proc, Dalian 116034, Peoples R China;[7]Dalian Polytech Univ, Dalian 116034, Peoples R China

年份：2021

卷号：12

期号：23

起止页码：11838

外文期刊名：FOOD & FUNCTION

收录：SCI-EXPANDED(收录号：WOS:000715376100001)、、EI(收录号：20214911288281)、Scopus(收录号：2-s2.0-85120540830)、WOS

基金：This work was co-supported by the National Key Research and Development Program (2019YFD0902004) and the Guangdong Innovation Team of Seafood Green Processing Technology (2019KCXTD011).

语种：英文

外文摘要：The oligopeptides derived from Auxis thazard protein (ATO) are a class of small peptides with molecular weight <1 kDa and good bioactivity. This paper aimed to explore the hypouricemic, hepatoprotective, and nephroprotective effects of ATO and its potential mechanisms in hyperuricemia in mice induced by potassium oxonate. The results showed that ATO significantly reduced serum UA, serum creatinine levels, inhibited XOD and ADA activities in the liver (p < 0.05), and accelerated UA excretion by downregulating the gene expression of renal mURAT1 and mGLUT9 and upregulating the gene expression of mABCG2 and mOAT1. ATO could also reduce the levels of liver MDA, increase the activities of SOD and CAT, and reduce the levels of IL-1 beta, MCP-1 and TNF-alpha. Histological analysis also showed that ATO possessed hepatoprotective and nephroprotective activities in hyperuricemic mice. Thus, ATO could reduce the serum UA level in hyperuricemic mice by decreasing UA production and promoting UA excretion from the kidney, suggesting that ATO could be developed as a dietary supplement for hyperuricemia treatment.