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Abstract：
This study aimed to investigate the potential mechanisms involved in the therapeutic effects of daitongxiao (DTX) on hyperuricemia (HUA). DTX was administered to two animal models of HUA via gavage feeding: HUA quail model (a uricotelic animal with urate oxidase deficiency), treated continuously for 35 days post-HUA induction, and HUA rats (an animal with active urate oxidase), treated continuously for 28 days post-HUA induction. HUA was induced in quail by administering a solution of sterile dry yeast powder via gavage feeding, while in rats, it was induced by intragastric gavage feeding of a solution of adenine and ethambutol hydrochloride. DTX improved overall health; increased bodyweight; reduced renal index, serum urate levels, serum xanthine oxidase activity, blood urea nitrogen, and creatinine; and enhanced urinary and fecal uric acid (UA) excretion in these two animal models. The results of hematoxylin and eosin and hexamine silver staining of kidney sections revealed that DTX significantly mitigated HUA-induced renal structural damage and inflammatory response. The results of quantitative real-time polymerase chain reaction, Western blotting, and immunofluorescence analyses revealed that DTX downregulated the renal expression levels of glucose transporter 9 (GLUT9) and upregulated the renal expression levels of organic anion transporters (OAT1 and OAT3) in both HUA models. Thus, the findings of this study suggest that DTX suppresses the progression of HUA by modulating the expression of the UA transporter group members.
摘要：
本研究旨在探讨大通消(DTX)治疗高尿酸血症(HUA)的潜在机制。通过管饲法将DTX给予两种HUA动物模型：HUA鹌鹑模型（一种尿酸氧化酶缺乏的泌尿动物），HUA诱导后连续治疗35天，和HUA大鼠（具有活性尿酸氧化酶的动物），在HUA诱导后连续治疗28天。HUA在鹌鹑中通过灌胃给药无菌干酵母粉溶液诱导，在老鼠身上，它是通过胃内管饲腺嘌呤和盐酸乙胺丁醇溶液诱导的。DTX改善了整体健康状况；增加了体重；降低了肾脏指数，血清尿酸水平，血清黄嘌呤氧化酶活性，血尿素氮,和肌酐；在这两种动物模型中，尿和粪便尿酸（UA）的排泄增加。肾脏切片的苏木精和伊红和六色银染色结果表明，DTX可显着减轻HUA诱导的肾脏结构损伤和炎症反应。定量实时聚合酶链反应的结果，西方印迹,和免疫荧光分析显示，DTX下调葡萄糖转运蛋白9（GLUT9）的肾脏表达水平，并上调两个HUA模型中有机阴离子转运蛋白（OAT1和OAT3）的肾脏表达水平。因此，这项研究的结果表明，DTX通过调节UA转运体组成员的表达来抑制HUA的进展。
