Negative correlation between serum uric acid and kidney URAT1 mRNA expression caused by resveratrol in rats

Lee, Cheng‐Tse; Chang, Li-Ching; Liu, Ching-Wen; Wu, Po-Han

doi:10.1002/mnfr.201601030

Cited by 21 publications

(15 citation statements)

References 26 publications

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“…The hyperuricemia rodent model can be induced through different inhibition pathways as follows. (1) Enhancement of the uric acid level in the body by the administration of uric acid directly [9], high-purine food such as fructose [10], or uric acid precursors, such as hypoxanthine (Hx) [11], which can produce uric acid to establish the model. (2) Inhibition of the excretion of uric acid through the kidneys.…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of Fucoidan and Fucoxanthin on Hyperuricemic Rats Induced by Potassium Oxonate

et al. 2019

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The purpose of this study was to investigate the preventive effects of fucoidan (Fc) and fucoxanthin (Fx) on hyperuricemic rats. Sprague Dawley (SD) rats were randomly assigned to seven groups: a control group, a hyperuricemia (HUA) group, low- and high-dose Fx groups, a Fc group, a combination Fc and Fx group, and a positive control group. Three weeks after the interventions, each group was given potassium oxonate (PO) and hypoxanthine (HX) to induce HUA in all groups except for the control group, and the rats were then sacrificed. Blood and urine were analyzed for biochemical properties, and differences in urine volume were determined. Livers and kidneys were collected to analyze xanthine oxidase (XO) activity and the expression of uric acid (UA) transporter-related proteins (GLUT9, ABCG2, OAT1, URAT1). The results show that HUA was successfully induced by PO/HX after 4 h of administration. The activity of XO was significantly reduced by a combination of Fc and Fx. In the combination group, both ABCG2 and OAT1 increased significantly, whereas GLUT9 and URAT1 decreased significantly. In summary, the combination of Fc and Fx can inhibit the activity of XO in the liver and regulate the expression of proteins related to UA transporter in the kidney to reduce the UA level in serum.

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Section: Discussionmentioning

confidence: 99%

Preventive Effects of Fucoidan and Fucoxanthin on Hyperuricemic Rats Induced by Potassium Oxonate

et al. 2019

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“…The mechanism of polyphenols inhibiting XO fruits, has been proved to reduce serum UA concentrations by up-regulating OAT1, down-regulating URAT1 and GLUT9 (Lee et al, 2017;Mehmood et al, 2019;Zhang et al, 2021). Additionally, the UA excretion transporter, ATP-binding cassette subfamily G member 2 (ABCG2), also plays an essential role in the excretion of UA.…”

Section: F I G U R E 3 the Classification Of Polyphenolsmentioning

confidence: 99%

A review on the fruit components affecting uric acid level and their underlying mechanisms

2021

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Uric acid (UA) is produced in the liver and excreted through the kidneys and intestines. If UA is overproduced or its excretion reduces, the concentration of UA increases, leading to hyperuricemia and gout. The high concentration of UA is also related to cardiovascular disease, hypertension, obesity, and other diseases. Fruits are healthy foods. However, fruits contain fructose and small amounts of purine, and the product of their metabolism is UA. Therefore, theoretically, eating fruits will increase the concentration of serum UA. Fruit components are numerous, and their effects on serum UA are complex. According to the current research, fructose, purine, polyphenols, vitamin C, dietary fiber, and minerals present in fruits influence serum UA concentrations. In addition to the UA synthesized by fructose and purine metabolism, the mechanisms by which other components affect the concentration of serum UA can be summarized as follows: (a) inhibiting xanthine oxidase; (b) reducing reabsorption of UA; and (c) improving the excretion of UA. In this review, we comprehensively discussed the fruit components that affect serum UA concentrations, and explained their mechanisms for the first time, which references for patients with hyperuricemia to take fruits. Practical applicationsWith the rising prevalence, hyperuricemia and gout have become public health problems that endanger our daily life. The key to the treatment of hyperuricemia is to control the level of serum UA within the normal range. Fruits are healthy foods.However, fruit components are numerous, and their effects on serum UA are complex. According to the current research, fructose, purine, polyphenols, vitamin C, dietary fiber, and minerals present in fruits influence serum UA concentrations. In this review, we comprehensively discussed the fruit components that affect serum UA concentrations. We also explained their mechanisms, which references for patients with hyperuricemia to take fruits.

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“…Numerous experimental studies and clinical trials have been conducted to analyze the systemic anti-inflammatory, antioxidative, multiorgan protective effects of resveratrol [13][14][15]. Our previous study explored the resveratrol is a potentially therapeutic strategy for hyperuricemia rats and disclosed immunoreactivity of IL-6 in renal cortex [16]. In this study, to evaluate how resveratrol regulates IL-6 in renal cells, pCMV6-IL-6 was overexpressed in the rat tubular epithelial cell line NRK-52E.…”

Section: Discussionmentioning

confidence: 97%

PI3K Signaling Pathway Regulates the Caspase-9 in Renal Tubular Epithelial Cells

2020

J Pharmacol Pharm Res

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Negative correlation between serum uric acid and kidney URAT1 mRNA expression caused by resveratrol in rats

Abstract: Resveratrol contributes to URAT1 expression, which is potentially useful in therapeutic strategies aimed at treating hyperuricemia.

Cited by 21 publications

References 26 publications

Preventive Effects of Fucoidan and Fucoxanthin on Hyperuricemic Rats Induced by Potassium Oxonate

Preventive Effects of Fucoidan and Fucoxanthin on Hyperuricemic Rats Induced by Potassium Oxonate

A review on the fruit components affecting uric acid level and their underlying mechanisms

PI3K Signaling Pathway Regulates the Caspase-9 in Renal Tubular Epithelial Cells

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