Previous studies have disclosed the antihyperuricemic effect of polydatin, a natural precursor of resveratrol; however, the mechanisms of action still remain elusive. The present study was undertaken to evaluate the therapeutic effects and the underlying mechanisms of polydatin on potassium oxonate-induced hyperuricemia in rats through metabonomic technology from a holistic view. Nuclear magnetic resonance (NMR) spectroscopy was applied to capture the metabolic changes in sera and urine collected from rats induced by hyperuricemia and polydatin treatment. With multivariate data analysis, significant metabolic perturbations were observed in hyperuricemic rats compared with the healthy controls. A total of eleven and six metabolites were identified as differential metabolites related to hyperuricemia in serum and urine of rats, respectively. The proposed pathways primarily included branched-chain amino acid (BCAA) metabolism, glycolysis, the tricarboxylic acid cycle, synthesis and degradation of ketone bodies, purine metabolism, and intestinal microflora metabolism. Additionally, some metabolites indicated the risk of renal injury induced by hyperuricemia. Polydatin significantly lowered the levels of serum uric acid, creatinine, and blood urea nitrogen and alleviated the abnormal metabolic status in hyperuricemic rats by partially restoring the balance of the perturbed metabolic pathways. Our findings shed light on the understanding of the pathophysiological process of hyperuricemia and provided a reference for revealing the metabolic mechanism produced by polydatin in the treatment of hyperuricemia.

中文翻译：

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基于NMR的代谢组学研究揭示了白藜芦醇苷对氧化钾诱导的大鼠高尿酸血症的干预作用。

先前的研究已经揭示了白藜芦醇的天然前体多糖polydatin的抗高尿酸作用。但是，作用机制仍然难以捉摸。本研究旨在通过代谢组学技术从整体的观点来评价白藜芦醇苷对草酸钾诱导的大鼠高尿酸血症的治疗作用及其潜在机制。应用核磁共振（NMR）光谱法捕获从高尿酸血症和多蛋白治疗引起的大鼠血清和尿液中的代谢变化。通过多变量数据分析，与健康对照组相比，在高尿酸血症大鼠中观察到明显的代谢紊乱。总共确定了11种和6种代谢物是与大鼠血清和尿液中高尿酸血症相关的差异代谢物。拟议的途径主要包括支链氨基酸（BCAA）代谢，糖酵解，三羧酸循环，酮体的合成和降解，嘌呤代谢和肠道菌群代谢。另外，一些代谢产物表明有高尿酸血症引起的肾损伤的危险。多肽抑制素通过部分恢复紊乱的代谢途径的平衡，显着降低了血尿酸，肌酐和血尿素氮的水平，减轻了高尿酸血症大鼠的异常代谢状态。我们的发现为对高尿酸血症的病理生理过程的理解提供了启示，并为揭示聚拉丁汀在高尿酸血症治疗中产生的代谢机制提供了参考。糖酵解，三羧酸循环，酮体的合成和降解，嘌呤代谢和肠道菌群代谢。另外，一些代谢产物表明有高尿酸血症引起的肾损伤的危险。多肽抑制素通过部分恢复紊乱的代谢途径的平衡，显着降低了血尿酸，肌酐和血尿素氮的水平，减轻了高尿酸血症大鼠的异常代谢状态。我们的发现为对高尿酸血症的病理生理过程的理解提供了启示，并为揭示聚拉丁汀在高尿酸血症治疗中产生的代谢机制提供了参考。糖酵解，三羧酸循环，酮体的合成和降解，嘌呤代谢和肠道菌群代谢。另外，一些代谢产物表明有高尿酸血症引起的肾损伤的危险。多肽抑制素通过部分恢复紊乱的代谢途径的平衡，显着降低了血尿酸，肌酐和血尿素氮的水平，减轻了高尿酸血症大鼠的异常代谢状态。我们的发现为对高尿酸血症的病理生理过程的理解提供了启示，并为揭示聚拉丁汀在高尿酸血症治疗中产生的代谢机制提供了参考。一些代谢产物表明高尿酸血症可引起肾损伤。多肽抑制素通过部分恢复紊乱的代谢途径的平衡，显着降低了血尿酸，肌酐和血尿素氮的水平，减轻了高尿酸血症大鼠的异常代谢状态。我们的发现为对高尿酸血症的病理生理过程的理解提供了启示，并为揭示聚拉丁汀在高尿酸血症治疗中产生的代谢机制提供了参考。一些代谢产物表明高尿酸血症可引起肾损伤。多肽抑制素通过部分恢复紊乱的代谢途径的平衡，显着降低了血尿酸，肌酐和血尿素氮的水平，减轻了高尿酸血症大鼠的异常代谢状态。我们的发现为对高尿酸血症的病理生理过程的理解提供了启示，并为揭示聚拉丁汀在高尿酸血症治疗中产生的代谢机制提供了参考。