Glut9在果糖诱导大鼠高尿酸血症中的作用

发布时间：2018-09-19 20:25

【摘要】：目的:观察肾脏转运蛋白葡萄糖转运体9(Glut9)与肾脏尿酸排泄的关系,探讨果糖诱导的高尿酸血症的病理机制。方法:将30只雄性SD大鼠按体质量随机分为正常组、模型组与苯溴马隆组,正常组给予清水,模型组与苯溴马隆组给予10%果糖饮水建立高尿酸血症模型。正常组与模型组给予清水灌胃,苯溴马隆组给予20 mg/kg苯溴马隆灌胃,实验第42天处死。检测大鼠血清尿酸和尿尿酸水平,计算肾脏尿酸清除率,并测定肝脏黄嘌呤氧化酶活性。利用免疫组化观察Glut9在各组大鼠肾脏的表达位点及其蛋白表达含量,实时荧光定量PCR(RT-q PCR)检测各组大鼠肾脏Glut9的mRNA表达水平。结果:实验第20~40天,与正常组比较,模型组的血尿酸水平显著升高,尿尿酸与尿酸清除率的差异无统计学显著性;实验第20天,与模型组比较,苯溴马隆组的血尿酸水平显著降低,但尿尿酸和尿酸清除率的差异无统计学显著性。实验第40天,模型组的肝脏黄嘌呤酶活性较正常组显著升高,但与模型组比较差异无统计学显著性。免疫组化实验结果显示,与正常组比较,模型组肾脏的Glut9蛋白表达显著增加;苯溴马隆组肾脏的Glut9蛋白表达少于模型组。RT-q PCR结果显示,各组肾脏Glut9 mRNA表达水平之间的差异并无统计学显著性。结论:10%果糖饮水可成功诱导大鼠高尿酸血症模型;果糖诱导高尿酸血症病理机制可能与上调肾脏Glut9蛋白水平、增加肾脏对尿酸的重吸收有关。
[Abstract]:Aim: to investigate the relationship between renal glucose transporter 9 (Glut9) and renal uric acid excretion and to explore the pathological mechanism of fructose induced hyperuricemia. Methods: thirty male SD rats were randomly divided into normal group, model group and benzyl bromide group, the normal group were given clear water, the model group and the benzbromarone group were given 10% fructose drinking water to establish hyperuricemia model. The normal group and the model group were fed with clear water and the benzyl bromide group was given 20 mg/kg of benzyl bromide Malone. The rats were killed on the 42nd day of the experiment. Serum uric acid and uric acid levels were measured, renal uric acid clearance rate and liver xanthine oxidase activity were calculated. The expression sites and protein expression of Glut9 in the kidney of rats in each group were observed by immunohistochemistry, and the mRNA expression of Glut9 in the kidney of each group was detected by real-time fluorescence quantitative PCR (RT-q PCR). Results: the level of serum uric acid in the model group was significantly higher than that in the normal group, and there was no significant difference in uric acid and uric acid clearance between the model group and the model group on the 20th day of the experiment, and on the 20th day of the experiment, the level of uric acid in the model group was significantly higher than that in the model group. The level of uric acid was significantly decreased in benzbromarone group, but there was no significant difference between uric acid and uric acid clearance. On the 40th day of the experiment, the activity of xanthine enzyme in the liver of the model group was significantly higher than that of the normal group, but there was no significant difference between the model group and the model group. The results of immunohistochemistry showed that the expression of Glut9 protein in kidney of model group was significantly higher than that of normal group, and the expression of Glut9 protein in kidney of benzimarone group was less than that of model group. RT-q PCR showed that the expression of Glut9 protein in model group was significantly higher than that in model group. There was no significant difference in the expression of Glut9 mRNA between the groups. Conclusion 10% fructose drinking water can successfully induce hyperuricemia in rats, and the pathological mechanism of fructose induced hyperuricemia may be related to upregulation of renal Glut9 protein level and increase of renal reabsorption of uric acid.
【作者单位】：北京中医药大学中药学院;
【基金】：北京市自然科学基金资助项目(No.7162117) 教育部高等学校博士学科点专项科研基金资助项目(No.20130013120001) 北京中医药大学研究生专项自主课题(No.2016-JYB-XS100)
【分类号】：R589.7

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