荷叶提取物对高尿酸血症的抑制作用及其可能机制

Yating An, Jia Hao, Jian Li, Wei He, Lei Wang, Yi Zhang
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引用次数: 2

摘要

摘要目的:荷叶是一种传统的中草药,几个世纪以来一直被成功地用于消肿利尿。基于其良好的临床证据和降压效果,本研究旨在探讨荷叶粗提物(LL)和荷叶总生物碱部位(LA)抑制高尿酸血症作用的潜在机制。方法:通过测定肝脏黄嘌呤氧化酶mRNA和蛋白的表达水平,分析LL和LA对黄嘌呤氧化酶(XOD)的体外抑制作用。在氧酸钾(PO)诱导的大鼠体内模型中,通过测定肾尿酸转运蛋白mRNA的表达,分析荷叶对高尿酸血症的抑制作用。结果:在40 μg/mL浓度下,LL和LA对XOD酶活性的抑制作用分别为37.35%±9.50%和47.73%±8.32%。l和LA均能显著降低po诱导的高尿酸血症大鼠血清和肝脏尿酸浓度。两种给药方式均能抑制XOD mRNA和蛋白表达,激活肾有机阴离子转运蛋白1/3 mRNA表达,并通过降低肾GLUT9和肾尿酸转运蛋白1抑制肾尿酸重吸收。结论:深入了解了LL和LA抑制高尿酸血症作用的机制。我们的研究结果表明,它们作用于两个目标:通过抑制肝脏中XOD的mRNA和蛋白表达来减少尿酸的产生,以及调节肾脏中肾尿酸转运蛋白的mRNA表达。
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The inhibitory effect of lotus leaf extract on hyperuricemia and its potential mechanism
Abstract Objective: Lotus leaf is a traditional Chinese herb that has been used successfully for centuries for relieving edema by inducing diuresis. Based on its good clinical evidence and anti-hypertensive effectiveness, this study aimed to investigate the potential mechanism of the hyperuricemic inhibitory effects of lotus leaf crude extract (LL) and lotus leaf total alkaloids fraction (LA). Methods: The xanthine oxidase (XOD) inhibitory effect of LL and LA was analyzed in vitro by determining mRNA expression and protein expression levels of hepatic XOD. The hyperuricemic inhibitory effect of the lotus leaf was analyzed in vivo in a potassium oxonate (PO)-induced rat model by determining mRNA expression for renal urate transporters. Results: At a concentration of 40 μg/mL, LL and LA suppressed XOD enzymatic activity by 37.35% ± 9.50% and 47.73% ± 8.32%, respectively. Both LL and LA administration significantly reduced the concentration of uric acid in the serum and liver of PO-induced hyperuricemic rats. Both LL and LA administration could inhibit XOD mRNA and protein expression, activate renal organic anion transporter 1/3 mRNA expression, and inhibit renal urate reabsorption by decreasing renal GLUT9 and renal urate transporter 1. Conclusions: Insight was gained into the mechanism behind the hyperuricemic inhibitory effects of LL and LA. Our results suggest that they act on two targets: decreasing the production of uric acid by inhibiting mRNA and protein expression of XOD in the liver, and regulating the mRNA expression of renal urate transporters in the kidneys.
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