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表没食子儿茶素没食子酸酯通过在体外和体内调节黄嘌呤氧化酶活性及尿酸排泄来降低尿酸水平。

Epigallocatechin gallate reduces uric acid levels by regulating xanthine oxidase activity and uric acid excretion in vitro and in vivo.

作者信息

Li Fang, Liu Yaping, Xie Yongyan, Liu Zhiyong, Zou Guoming

机构信息

Jiangxi Maternal and Child Health Hospital, Nanchang 330006, China.

Jiangxi University of Traditional Chinese Medicine, Nanchang 330003, China.

出版信息

Ann Palliat Med. 2020 Mar;9(2):331-338. doi: 10.21037/apm.2019.11.28. Epub 2019 Dec 22.

Abstract

BACKGROUND

This study investigates the effect of epigallocatechin gallate (EGCG) from tea leaves on hyperuricemia and explores the underlying mechanisms in vitro and in vivo.

METHODS

The effects of EGCG on proliferation of BRL 3A rat liver cells were evaluated by CCK8 and after stimulation by xanthine the uric acid and xanthine oxidase (XOD) levels were evaluated by a kit; In an in vivo experiment, rats were treated with oxonic acid potassium salt combined with ethylamine pyrimidine to induce high uric acid hematic disease (7 days), The serum uric acid levels and XOD levels were evaluated by a kit, The expressions of OTA1 and GLUT9 were detected by RT-qPCR and Immunohistochemical.

RESULTS

EGCG had no effect on proliferation, and significantly reduced serum uric acid levels and inhibited XOD activity (P<0.05). The rat model exhibited a significant rise in blood uric acid levels (54.59 mg/dL), and EGCG significantly reduced the high level of serum uric acid and inhibited XOD activity in the serum and liver tissues (P<0.05). RT-PCR showed that EGCG significantly increased mOAT1 expression in the kidney tissues and reduced mGLUT9 expression (P<0.05). Immunohistochemical results showed that EGCG significantly increased OAT1 expression in the kidney tissues and decreased GLUT9 expression (P<0.05).

CONCLUSIONS

These results demonstrate that EGCG has obvious anti-hyperuricemia effects in vitro and in vivo via the inhibition of XOD activity and GLUT9 expression and the promotion of OAT1 expression.

摘要

背景

本研究调查茶叶中的表没食子儿茶素没食子酸酯(EGCG)对高尿酸血症的影响,并在体外和体内探索其潜在机制。

方法

通过CCK8评估EGCG对BRL 3A大鼠肝细胞增殖的影响,在用黄嘌呤刺激后,使用试剂盒评估尿酸和黄嘌呤氧化酶(XOD)水平;在体内实验中,用氧嗪酸钾盐联合乙胺嘧啶处理大鼠以诱导高尿酸血症(7天),使用试剂盒评估血清尿酸水平和XOD水平,通过RT-qPCR和免疫组织化学检测OTA1和GLUT9的表达。

结果

EGCG对增殖无影响,但显著降低血清尿酸水平并抑制XOD活性(P<0.05)。大鼠模型的血尿酸水平显著升高(54.59mg/dL),而EGCG显著降低血清尿酸的高水平,并抑制血清和肝组织中的XOD活性(P<0.05)。RT-PCR显示,EGCG显著增加肾组织中mOAT1的表达并降低mGLUT9的表达(P<0.05)。免疫组织化学结果显示,EGCG显著增加肾组织中OAT1的表达并降低GLUT9的表达(P<0.05)。

结论

这些结果表明,EGCG在体外和体内均具有明显的抗高尿酸血症作用,其机制是通过抑制XOD活性和GLUT9表达以及促进OAT1表达来实现的。

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