The spice clove effectively ameliorated hyperuricemia and hyperuricemia-induced kidney injury in mice
Clove, the dried flower bud of Syzygium aromaticum, is a global spice used in various culinary traditions. In the present study, the antihyperuricemic (anti-HUA) effect of a clove water extract (CWE) and its mechanism were investigated using a hyperuricemic (HUA) mouse model, with organ coefficients...
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| Main Authors: | , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-04-01
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| Series: | Journal of Agriculture and Food Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2666154325001310 |
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| Summary: | Clove, the dried flower bud of Syzygium aromaticum, is a global spice used in various culinary traditions. In the present study, the antihyperuricemic (anti-HUA) effect of a clove water extract (CWE) and its mechanism were investigated using a hyperuricemic (HUA) mouse model, with organ coefficients and histological assessments employed to determine its safety profile. Western blot, RT-qPCR and transcriptomic analysis were conducted to uncover the proteins, RNAs and signalling pathways involved. The results showed that a very low dose of clove water extract could significantly lower serum uric acid (UA) levels in HUA mice with no overt toxicity to the organs and markedly attenuated HUA-induced renal damage. Western blotting analysis revealed that the expression levels of xanthine oxidase (XOD), urate transporter 1 (URAT1), glucose transporter 9 (GLUT9), and monocarboxylate transporter 9 (MCT9) were substantially decreased, whereas those of renal organic anion transporters 1 (OAT1) and 3 (OAT3) and ATP transporter G2 (ABCG2) were notably increased. Transcriptomic analysis revealed that CWE reversed 38 differentially expressed key genes within the kidney induced by HUA. A reduction in the expression of inflammatory cytokines and their transcription factors in the cytokine‒cytokine receptor interaction signalling pathway was also observed. The UA-lowering mechanism of CWE involved suppressing XOD to curtail UA synthesis; lowering the expression of URAT1, GLUT9, and MCT9 to diminish UA reabsorption; and enhancing the expression of ABCG2, OAT1, and OAT3 to increase UA elimination. Additionally, CWE is capable of mitigating HUA-induced kidney injury through modulating the cytokine‒cytokine receptor interaction signalling pathway. |
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| ISSN: | 2666-1543 |