【摘要】：目的:觀察腎臟轉(zhuǎn)運(yùn)蛋白葡萄糖轉(zhuǎn)運(yùn)體9(Glut9)與腎臟尿酸排泄的關(guān)系,探討果糖誘導(dǎo)的高尿酸血癥的病理機(jī)制。方法:將30只雄性SD大鼠按體質(zhì)量隨機(jī)分為正常組、模型組與苯溴馬隆組,正常組給予清水,模型組與苯溴馬隆組給予10%果糖飲水建立高尿酸血癥模型。正常組與模型組給予清水灌胃,苯溴馬隆組給予20 mg/kg苯溴馬隆灌胃,實(shí)驗(yàn)第42天處死。檢測大鼠血清尿酸和尿尿酸水平,計(jì)算腎臟尿酸清除率,并測定肝臟黃嘌呤氧化酶活性。利用免疫組化觀察Glut9在各組大鼠腎臟的表達(dá)位點(diǎn)及其蛋白表達(dá)含量,實(shí)時(shí)熒光定量PCR(RT-q PCR)檢測各組大鼠腎臟Glut9的mRNA表達(dá)水平。結(jié)果:實(shí)驗(yàn)第20~40天,與正常組比較,模型組的血尿酸水平顯著升高,尿尿酸與尿酸清除率的差異無統(tǒng)計(jì)學(xué)顯著性;實(shí)驗(yàn)第20天,與模型組比較,苯溴馬隆組的血尿酸水平顯著降低,但尿尿酸和尿酸清除率的差異無統(tǒng)計(jì)學(xué)顯著性。實(shí)驗(yàn)第40天,模型組的肝臟黃嘌呤酶活性較正常組顯著升高,但與模型組比較差異無統(tǒng)計(jì)學(xué)顯著性。免疫組化實(shí)驗(yàn)結(jié)果顯示,與正常組比較,模型組腎臟的Glut9蛋白表達(dá)顯著增加;苯溴馬隆組腎臟的Glut9蛋白表達(dá)少于模型組。RT-q PCR結(jié)果顯示,各組腎臟Glut9 mRNA表達(dá)水平之間的差異并無統(tǒng)計(jì)學(xué)顯著性。結(jié)論:10%果糖飲水可成功誘導(dǎo)大鼠高尿酸血癥模型;果糖誘導(dǎo)高尿酸血癥病理機(jī)制可能與上調(diào)腎臟Glut9蛋白水平、增加腎臟對尿酸的重吸收有關(guān)。
[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.
【作者單位】： 北京中醫(yī)藥大學(xué)中藥學(xué)院;
【基金】：北京市自然科學(xué)基金資助項(xiàng)目(No.7162117) 教育部高等學(xué)校博士學(xué)科點(diǎn)專項(xiàng)科研基金資助項(xiàng)目(No.20130013120001) 北京中醫(yī)藥大學(xué)研究生專項(xiàng)自主課題(No.2016-JYB-XS100)
【分類號(hào)】：R589.7

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