别嘌醇可降低果糖诱导的高尿酸血症大鼠的血清尿酸水平及肠道葡萄糖转运蛋白5的表达。
Allopurinol decreases serum uric acid level and intestinal glucose transporter-5 expression in rats with fructose-induced hyperuricemia.
作者信息
Chen Gang, Jia Ping
机构信息
Chongqing Key Laboratory of Nature Medicine Research, College of Environment and Resources, Chongqing Technology and Business University, Chongqing, China; Chongqing Key Lab of Catalysis and Functional Organic Molecules, College of Environment and Resource, Chongqing Technology and Business University, Chongqing, China.
Department of Combination of Chinese and Western Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
出版信息
Pharmacol Rep. 2016 Aug;68(4):782-6. doi: 10.1016/j.pharep.2016.04.014. Epub 2016 May 6.
BACKGROUND
High fructose consumption is considered to be related to the increasing prevalence of hyperuricemia (HUA). Glucose transporters (GLUT) 2 and 5 are crucial for fructose absorption and transporter. Effects of anti-HUA drugs, allopurinol (API) and benzbromarone (BBR), on expressions of GLUT5 and GLUT2 are not evaluated.
METHOD
Wistar rats were given 10% fructose in drinking water for 60 days to induce HUA, and 5mg/kg API and 10mg/kg BBR were intragastricly treated for 30 days. Serum level of uric acid and xanthine oxidase (XOD) activity in liver were determined. Expressions of GLUT2 and GLUT5 in intestine were analyzed by immunohistochemistry staining assay and Western blot assay.
RESULTS
Treatment with API or BBR significantly decreased the serum level of uric acid in HUA rats induced by fructose. Meanwhile, API treatment significantly reduced the XOD activity in liver and GLUT5 expression in intestine. However, BBR treatment did not show inhibitory effects on hepatic XOD activity and intestinal GLUT5 expression. In addition, treatment with API or BBR did not show any effect on GLUT2 expression in intestine.
CONCLUSION
API decreases serum level of uric acid in fructose-induced HUA rats. The mechanisms are associated with suppressing XOD activity in liver to reduce uric acid production, and inhibiting GLUT5 expression in intestine to reduce fructose absorption.
背景
高果糖摄入被认为与高尿酸血症（HUA）患病率的增加有关。葡萄糖转运蛋白（GLUT）2和5对果糖的吸收和转运至关重要。抗HUA药物别嘌醇（API）和苯溴马隆（BBR）对GLUT5和GLUT2表达的影响尚未评估。
方法
给Wistar大鼠饮用含10%果糖的水60天以诱导HUA，然后分别用5mg/kg API和10mg/kg BBR灌胃治疗30天。测定血清尿酸水平和肝脏中的黄嘌呤氧化酶（XOD）活性。通过免疫组织化学染色法和蛋白质印迹法分析肠道中GLUT2和GLUT5的表达。
结果
用API或BBR治疗可显著降低果糖诱导的HUA大鼠的血清尿酸水平。同时，API治疗可显著降低肝脏中的XOD活性和肠道中的GLUT5表达。然而，BBR治疗对肝脏XOD活性和肠道GLUT5表达没有抑制作用。此外，用API或BBR治疗对肠道中GLUT2的表达没有任何影响。
结论
API可降低果糖诱导的HUA大鼠的血清尿酸水平。其机制与抑制肝脏中的XOD活性以减少尿酸生成，以及抑制肠道中的GLUT5表达以减少果糖吸收有关。
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