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茶及其成分通过抑制黄嘌呤氧化酶来减少尿酸的产生。

Tea and its components reduce the production of uric acid by inhibiting xanthine oxidase.

作者信息

Wu Dan, Chen Ruohong, Zhang Wenji, Lai Xingfei, Sun Lingli, Li Qiuhua, Zhang Zhenbiao, Cao Junxi, Wen Shuai, Lai Zhaoxiang, Li Zhigang, Cao Fanrong, Sun Shili

机构信息

Tea Research Institute, Guangdong Academy of Agricultural Sciences/Guangdong Provincial Key Laboratory of Tea Plant Resources Innovation & Utilization, Guangzhou, China.

College of Horticulture, South China Agricultural University, Guangzhou, China.

出版信息

Food Nutr Res. 2022 Jun 15;66. doi: 10.29219/fnr.v66.8239. eCollection 2022.

DOI:10.29219/fnr.v66.8239
PMID:35844955
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9250135/
Abstract

BACKGROUND

The health benefits of tea are as diverse including the reduction of uric acid levels. Xanthine oxidase is the most directly mediated enzyme in the production of uric acid.

OBJECTIVE

To explore the inhibitory effects of different teas and its main bioactive components on the production of uric acid.

DESIGN

Experimental study. The experiments were conducted in vitro using human immortalized normal liver cell line HL-7702 (L-02).

RESULTS

The inhibition of the xanthine oxidase activities and the expression level of xanthine dehydrogenase mRNA stimulated in the hyperuric hepatocyte cell model showed that the unfermented green tea and th1e lightly fermented yellow tea, white tea, and oolong tea significantly stronger than the highly fermented black tea and dark tea. The main bioactive compound, gallic acid, showed the strongest inhibitory effect on uric acid production, followed by tea polyphenols and theaflavins.

DISCUSSION

All teas exhibited significant inhibition of xanthine oxidase activities, and the degree of fermentation of tea may be inversely proportional to its ability to inhibit the production of uric acid. Compared with tea polyphenols rich in tea, gallic acid may be a more potential uric acid-lowering component.

CONCLUSION

In this article, we first compared the effects of six traditional Chinese tea made from a single variety in stabilizing the synthesis of uric acid and found that the lighter the fermentation, the greater the potential for inhibiting the production of uric acid. Furthermore, we analyzed the inhibitory effects of its main biochemical active ingredients and found that the inhibitory effects of polyphenols rich in lightly fermented tea were significantly stronger than caffeine rich in highly fermented tea. Our findings will be helpful for people to choose a proper tea for alleviating hyperuricemia and provide a scientific basis for uric acid-lowering tea processing.

摘要

背景

茶对健康的益处多种多样,包括降低尿酸水平。黄嘌呤氧化酶是尿酸生成过程中最直接介导的酶。

目的

探讨不同茶叶及其主要生物活性成分对尿酸生成的抑制作用。

设计

实验研究。实验在体外使用人永生化正常肝细胞系HL-7702(L-02)进行。

结果

在高尿酸肝细胞模型中,对黄嘌呤氧化酶活性的抑制以及黄嘌呤脱氢酶mRNA表达水平的刺激表明,未发酵的绿茶以及轻度发酵的黄茶、白茶和乌龙茶的抑制作用明显强于高度发酵的红茶和黑茶。主要生物活性化合物没食子酸对尿酸生成的抑制作用最强,其次是茶多酚和茶黄素。

讨论

所有茶叶均对黄嘌呤氧化酶活性表现出显著抑制作用,茶的发酵程度可能与其抑制尿酸生成的能力成反比。与茶叶中富含的茶多酚相比,没食子酸可能是更具潜力的降尿酸成分。

结论

在本文中,我们首次比较了单一品种制成的六种中国传统茶对稳定尿酸合成的影响,发现发酵程度越轻,抑制尿酸生成的潜力越大。此外,我们分析了其主要生化活性成分的抑制作用,发现轻度发酵茶中富含的多酚类物质的抑制作用明显强于高度发酵茶中富含的咖啡因。我们的研究结果将有助于人们选择合适的茶来缓解高尿酸血症,并为降尿酸茶的加工提供科学依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/674ebe56668f/FNR-66-8239-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/01339f263319/FNR-66-8239-ug001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/9e5b1e1d4820/FNR-66-8239-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/887c95ee7e92/FNR-66-8239-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/c463bd116b4f/FNR-66-8239-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/afb90665ade5/FNR-66-8239-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/187fd4356ba7/FNR-66-8239-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/af1733d33757/FNR-66-8239-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/45d6157e06d3/FNR-66-8239-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/674ebe56668f/FNR-66-8239-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/01339f263319/FNR-66-8239-ug001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/9e5b1e1d4820/FNR-66-8239-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/887c95ee7e92/FNR-66-8239-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/c463bd116b4f/FNR-66-8239-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/afb90665ade5/FNR-66-8239-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/187fd4356ba7/FNR-66-8239-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/af1733d33757/FNR-66-8239-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/45d6157e06d3/FNR-66-8239-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0f5/9250135/674ebe56668f/FNR-66-8239-g008.jpg

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