Molecules (Nov 2022)

The Therapeutic Effect and the Potential Mechanism of Flavonoids and Phenolics of <i>Moringa oleifera</i> Lam. Leaves against Hyperuricemia Mice

  • Xiaowei Luo,
  • Lipeng Zhou,
  • Shukai Wang,
  • Jing Yuan,
  • Zihao Chang,
  • Qian Hu,
  • Yinxin Chen,
  • Yuqi Liu,
  • Ya Huang,
  • Baojin Wang,
  • Ye Gao,
  • Zhaohui Wang,
  • Yitong Cui,
  • Yue Liu,
  • Lanzhen Zhang

DOI
https://doi.org/10.3390/molecules27238237
Journal volume & issue
Vol. 27, no. 23
p. 8237

Abstract

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The aim of this study is to evaluate the anti-hyperuricemia effect and clarify the possible mechanisms of flavonoids and phenolics of MOL (MOL-FP) in mice. Hyperuricemia mice were generated via intraperitoneal (i.p.) administration of potassium oxonate (PO) and oral gavage (p.o.) of hypoxanthine (HX). Serum uric acid (UA), weight, serum XO activity, hepatic XO activity, urea nitrogen (BUN), creatinine (CRE), serum AST level, serum ALT level, mRNA expression of renal urate-anion transporter 1 (URAT1), glucose transporter 9 (GLUT9), organic anion transporters 1 (OAT1), organic anion transporters 3 (OAT3), and ATP-binding cassette transporter G2 (ABCG2) were determined. The molecular docking was conducted using AutoDock Vina 1.2.0 to screen potential XO inhibitors in MOL-FP. Serum metabolomics was established to collect the metabolic profiles of mice and explore the metabolic changes that occurred after MOL-FP treatment. MOL-FP could notably reduce the serum UA level of hyperuricemia mice by inhibiting XO activity and regulating renal urate transporters. Molecular docking studies indicated that 5-p-coumaroylquinic acid, 3-p-coumaroylquinic acid, and catechin could be potential XO inhibitors. Besides, MOL-FP prevented the pathological process of hyperuricemia by regulating biomarkers associated with purine metabolism, amino acid metabolism, and lipid metabolism.

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