摘要
目的观察茶多酚(green tea polyphenols,GTP)对氧嗪酸钾(PO)诱导的高尿酸血症(HUA)小鼠血尿酸水平的影响,并从调节尿酸产生和排泄途径探讨其药理机制。方法每天分别灌胃给予PO(250 mg·kg^(-1))和GTP(150、300、600mg·kg^(-1)),连续7 d。磷钨酸法检测小鼠血尿酸水平,比色法和Western blot法分别检测肝脏黄嘌呤氧化酶(XOD)活性与表达,免疫组织化学染色法检测肾脏中尿酸盐转运子1(URAT1)、有机阴离子转运子(OAT)1和3的表达。结果GTP明显降低了氧嗪酸钾诱导的HUA小鼠血尿酸水平(P<0.05或P<0.01);同时,GTP明显降低了HUA小鼠肝脏XOD的活性和表达(P<0.05或P<0.01);此外,GTP还明显降低了HUA小鼠肾脏URAT1的表达,增强了OAT1和OAT3的表达(P<0.05或P<0.01)。结论 GTP对PO诱导的HUA小鼠血尿酸水平有明显降低作用,其机制与减少尿酸产生和增加尿酸排泄密切相关。
Aim To investigate the effect of green tea polyphenols（GTP）on serum level of uric acid in potas-sium oxonate （PO）-induced hyperuricemic mice,and explore the potential mechanism.Methods PO and GTP were intragastricly administered to mice for seven consecutive days.Uric acid level in serum was exam-ined.Meanwhile,activity and expressions of xanthine oxidase（XOD）in liver were tested.In additon,ex-pressions of urate transporters including urate-anion transporter （URAT ） 1 , organic anion transporter （OAT）1 and 3 in kidney were analyzed.Results GTP significantly decreased the serum level of uric acid in PO-induced hyperuricemic mice.At the same time, GTP markedly reduced the activity and expression of XOD in liver of hyperuricemic mice.Finally,GTP markedly reduced the expression of URAT1 ,OAT1 and OAT3 in kidney of hyperuricemic mice.Conclusion GTP has the effect of lowering uric acid in PO-induced hyperuricemic mice through both decreasing the uric acid production and increasing uric acid excretion.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2017年第2期218-222,共5页
Chinese Pharmacological Bulletin
基金
重庆市教委科学技术研究项目(NoKJ1400626)
重庆市科委前沿与应用基础研究项目(Nocstc2016jcyja0475)
作者简介
陈刚（1974-）,男,博士,副教授,研究方向：高尿酸血症与痛风的发病机制与药物防治,通讯作者,E-mail：lico-ricech@ctbu.edu.cn
