摘要
该研究以氧嗪酸钾诱导的高尿酸血症小鼠模型为对象,来评价不同剂量大鲵骨肽(Andrias davidianus bone peptides,ADBP)[150 mg/(kg·bw)、300 mg/(kg·bw)和600 mg/(kg·bw)]降尿酸功效。结果表明,ADBP可显著降低血清中尿酸(uric acid,UA)、肌酐和尿素氮水平,有效抑制UA合成相关酶,黄嘌呤氧化酶(xanthine oxidas,XOD)和腺苷脱氨酶的活力,下调高尿酸血症小鼠肝脏中XOD的mRNA表达水平。ADBP通过调节氧化应激(总抗氧化能力、超氧化物歧化酶、谷胱甘肽过氧化物酶、丙二醛含量),抑制促炎细胞因子(CXCL1、IL-1β、IL-6、TNF-α)水平,改善了肝脏和肾脏的组织病理学损伤。研究证实ADBP对高尿酸血症小鼠有明显的降尿酸作用,对长期高尿酸引起的机体损伤有一定的修复作用,可作缓解和治疗高尿酸血症的物质。
In this study,the uric acid-lowering effects of Andrias davidianus bone peptides(ADBP)at different doses were evaluated in a mouse model of hyperuricemia induced by potassium oxonate,including 150 mg/(kg·bw),300 mg/(kg·bw),and 600 mg/(kg·bw).Results revealed that ADBP significantly reduced the levels of uric acid(UA),creatinine(CRE),and blood urea nitrogen(BUN)in serum,and effectively suppressed the activities of xanthine oxidase(XOD)associated with UA synthesis.Furthermore,it down-regulated the expression level of XOD mRNA in the liver of hyperuricemia mice.ADBP regulated oxidative stress(total antioxidant,superoxide dismutase,glutathione peroxidase,and malondialdehyde)and inhibited pro-inflammatory cytokines(CXCL1,IL-1β,IL-6,and TNF-α),resulting in improved histopathological damage in the liver and kidneys.Studies have confirmed that ADBP had a significant uric acid-lowering effect on hyperuricemia mice and could repair long-term damage caused by high uric acid.Therefore,it can be used to relieve and treat hyperuricemia.
作者
郑小莉
陈德经
苏文
江海
曾允灏
祁珊珊
ZHENG Xiaoli;CHEN Dejing;SU Wen;JIANG Hai;ZENG Yunhao;QI Shanshan(School of Biological Science and Engineering,Shaanxi University of Technology,Hanzhong 723001,China;Shaanxi Provincial Key Laboratory of Resource Biology,Shaanxi University of Technology,Hanzhong 723001,China)
出处
《食品与发酵工业》
北大核心
2025年第8期267-275,共9页
Food and Fermentation Industries
基金
陕西理工大学“市校共建”科研专项(SXZC202101)。
关键词
大鲵骨肽
黄嘌呤氧化酶
高尿酸血症
氧化应激
炎症因子
Andrias davidianus bone peptides
xanthine oxidase
hyperuricemia
oxidative stress
inflammatory factors
作者简介
第一作者:郑小莉,硕士研究生;通信作者:陈德经,授,E-mail:cdjslg@126.com。
