Riparoside B and timosaponin J, two steroidal glycosides from Smilax riparia, resist to hyperuricemia based on URAT1 in hyperuricemic mice

Wu, Xiao Hui; Zhang, Jun; Wang, Shu Qing; Yang, Victor C.; Anderson, Samantha; Zhang, Yan Wen

doi:10.1016/j.phymed.2014.03.009

Cited by 33 publications

(18 citation statements)

References 18 publications

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“…7, instead of vice versa. In the present study, potassium oxonate-induced hyperuricemic rats developed the elevated levels of renal URAT1 and GLUT9 protein and depressed OTA1protein levels compared with normal-vehicle rats, which is consistent with the results of various studies [51-53], but the mechanism involved is not clear.…”

Section: Discussionsupporting

confidence: 90%

Hypouricemic and Nephroprotective Effects of an Active Fraction from Polyrhachis Vicina Roger On Potassium Oxonate-Induced Hyperuricemia in Rats

Nong

et al. 2018

Kidney Blood Press Res

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Background/Aims: The objective of this study is to evaluate the hypouricemic and nephroprotective effects of an active fraction from Polyrhachis vicina Roger (AFPR) in potassium oxonate-induced hyperuricemic rats. Methods: Hyperuricemia was induced by potassium oxonate in male rats. AFPR was orally administered to hyperuricemic rats for 12 consecutive weeks. Serum, liver and kidney samples were collected for effects and mechanism analysis. The levels of serum uric acid (SUA) were measured by the phosphotungstic acid method, xanthine oxidase (XOD) activity in the hepatic and serum samples were measured by ultraviolet spectrophotometry, serum levels of interleukin-1 (IL-1β), interleukin-1 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by ELISA, the levels of serum creatinine (SCr), blood urea nitrogen (BUN), super oxide dismutase (SOD) and malondialdehyde (MDA) in serum were determined by colorimetric method. Protein expression of renal URAT1, GLUT9, and OAT1 were analyzed by Western blot. Results: AFPR significantly decreased the levels of SUA, serum and hepatic XOD, SCr, BUN, and MDA as well as increased SOD. In addition, AFPR treatment significantly reduced the levels of proinflammatory cytokines in serum, including IL-1β, IL-6 and TNF-α. Moreover, we found the significant decrease in protein expression of URAT1 and GLUT9, and the significant increase in protein expression of OAT1 in the kidney in AFPR treated groups compared to the model groups of hyperuricemia. Conclusion: These findings suggest that AFPR has anti-hyperuricemic activity attributed to the inhibition of uric acid generation in the liver and probably to the enhancement of urate excretion in the kidney, and possess nephroprotective effect in hyperuricemic rats due to its anti-inflammatory and antioxidant activities.

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Section: Discussionsupporting

confidence: 90%

Hypouricemic and Nephroprotective Effects of an Active Fraction from Polyrhachis Vicina Roger On Potassium Oxonate-Induced Hyperuricemia in Rats

Nong

et al. 2018

Kidney Blood Press Res

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“…Moreover, they also isolated riparoside B and timosaponin J from S. riparia . These two compounds exhibited XOD inhibitory activities (Figure ) (Wu, Zhang, et al., ).…”

Section: Natural Compounds: As a Xanthine Oxidase Inhibitorsmentioning

confidence: 98%

Natural compounds with xanthine oxidase inhibitory activity: A review

et al. 2019

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Hyperuricemia (HUA), a disease due to an elevation of body uric acid level and responsible for various diseases such as gout, cardiovascular disorders, and renal failure, is a major ground debate for the medical science these days. Considering the risk factors linked with allopathic drugs for the treatment of this disease, the debate has now become a special issue. Previously, we critically discussed the role of dietary polyphenols in the treatment of HUA. Besides dietary food plants, many researchers figure out the tremendous effects of medicinal plants‐derived phytochemicals against HUA. Keeping in mind all these aspects, we reviewed all possible managerial studies related to HUA through medicinal plants (isolated compounds). In the current review article, we comprehensively discussed various bioactive compounds, chemical structures, and structure–activity relationship with responsible key enzyme xanthine oxidase.

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“…Hyperuricemia, the deposition of urate crystals in the joints caused by high uric acid level in the blood (Wu et al, 2014), could result from either overproduction of uric acid (10% of hyperuricemic cases), or from lowered uric acid excretion (90% of cases), or both (Wolff, Cruz, Vanderman, & Brown, 2015). Hyperuricemia in adults could ensue when blood uric acid is more than 7 mg/dl in men and 6 mg/dl in women.…”

Section: Introductionmentioning

confidence: 99%

Possible role ofl‐carnitine in improvement of metabolic and hepatic changes in hyperuricemic and hyperuricemic—Fructose‐supplemented rats

et al. 2019

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Hyperuricemia was linked to diabetes mellitus, metabolic syndrome, and oxidative stress, and could be induced by higher fructose consumption through altering energy status in liver. l‐Carnitine is an antioxidant, affecting mitochondria and cellular energetics; however, little is known about its effects in hyperuricemic states. This study investigated metabolic and hepatic effects of hyperuricemia and fructose feeding, and demonstrated the role of l‐Carnitine in such states. Fifty adult male Wistar rats were randomly divided into control, untreated hyperuricemic, fructose‐supplemented hyperuricemic, l‐Carnitine‐treated hyperuricemic, and l‐Carnitine‐treated fructose‐supplemented hyperuricemic groups. The separated plasma was used for determination of the glycemic control, lipid profile, liver function tests, uric acid level, and oxidative stress markers. Atherogenic index, HOMA‐IR, and body mass index (BMI) were calculated. Left liver lobe and left kidney specimen from all groups were used for histopathological studies. Hyperuricemic rats exhibited significantly hypoalbuminemia, dyslipidemia, insulin resistance, and oxidative stress compared to the controls. Fructose‐supplemented hyperuricemic group showed obesity and more deleterious effects, as well as, steatosis, and renal tubular damage compared to the hyperuricemic rats. Concomitant l‐Carnitine treatment with hyperuricemia improved such effects, despite causing adiposity. While combined l‐Carnitine treatment and fructose supplementation in hyperuricemia limited the aggressive hyperuricemic picture of fructose supplementation. It is concluded that hyperuricemia has detrimental metabolic and hepatic effects. Artificial fructose supplementation worsened such effects, while l‐Carnitine was efficient in ameliorating these hyperuricemia and/or excess fructose‐induced hyperuricemia effects, through its anti‐inflammatory, antisteatotic, and antioxidant properties.

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Riparoside B and timosaponin J, two steroidal glycosides from Smilax riparia, resist to hyperuricemia based on URAT1 in hyperuricemic mice

Cited by 33 publications

References 18 publications

Hypouricemic and Nephroprotective Effects of an Active Fraction from <b><i>Polyrhachis Vicina Roger</i></b> On Potassium Oxonate-Induced Hyperuricemia in Rats

Hypouricemic and Nephroprotective Effects of an Active Fraction from <b><i>Polyrhachis Vicina Roger</i></b> On Potassium Oxonate-Induced Hyperuricemia in Rats

Natural compounds with xanthine oxidase inhibitory activity: A review

Possible role ofl‐carnitine in improvement of metabolic and hepatic changes in hyperuricemic and hyperuricemic—Fructose‐supplemented rats

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