scholarly journals DKB114, A Mixture of Chrysanthemum Indicum Linne Flower and Cinnamomum Cassia (L.) J. Presl Bark Extracts, Improves Hyperuricemia through Inhibition of Xanthine Oxidase Activity and Increasing Urine Excretion

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1381 ◽  
Author(s):  
Young-Sil Lee ◽  
Seung-Hyung Kim ◽  
Heung Yuk ◽  
Dong-Seon Kim

Chrysanthemum indicum Linne flower (CF) and Cinnamomum cassia (L.) J. Presl bark (CB) extracts have been used as the main ingredients in several prescriptions to treat the hyperuricemia and gout in traditional medicine. In the present study, we investigated the antihyperuricemic effects of DKB114, a CF, and CB mixture, and the underlying mechanisms in vitro and in vivo. DKB114 markedly reduced serum uric acid levels in normal rats and rats with PO-induced hyperuricemia, while increasing renal uric acid excretion. Furthermore, it inhibited the activity of xanthine oxidase (XOD) in vitro and in the liver in addition to reducing hepatic uric acid production. DKB114 decreased cellular uric acid uptake in oocytes and HEK293 cells expressing human urate transporter (hURAT)1 and decreased the protein expression levels of urate transporters, URAT1, and glucose transporter, GLUT9, associated with the reabsorption of uric acid in the kidney. DKB114 exerts antihyperuricemic effects and uricosuric effects, which are accompanied, partially, by a reduction in the production of uric acid and promotion of uric acid excretion via the inhibition of XOD activity and reabsorption of uric acid. Therefore, it may have potential as a treatment for hyperuricemia and gout.

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Young-Sil Lee ◽  
Eunjung Son ◽  
Seung-Hyung Kim ◽  
Yun Mi Lee ◽  
Ohn Soon Kim ◽  
...  

Chrysanthemum indicum Linne flower (CF) and Cinnamomum cassia (L.) J. Persl bark (CB) extracts have served as the main ingredients in several prescriptions designed to treat hyperuricemia and gout in traditional Chinese and Korean medicine. However, little is known about the combination effects of a CF and CB (CC) mixture on hyperuricemia. In our study, we investigated the antihyperuricemic effects of CC mixture and the mechanisms underlying these effects in normal and potassium oxonate- (PO-) induced hyperuricemic rats. The CC mixture significantly decreased uric acid levels in normal and PO-induced hyperuricemic rats and showed the enhanced hypouricemic effect compared to CF or CB alone. Furthermore, the CC mixture increased renal uric acid excretion in PO-induced hyperuricemic rat. We found that CC mixture and its major components, chlorogenic acid, 3,4-dicaffeoylquinic acid (isochlorogenic acid), coumarin, cinnamaldehyde, trans-cinnamic acid, and o-methoxycinnamaldehyde, inhibit the activity of xanthine oxidase (XOD) in vitro. The CC mixture exerts antihyperuricemic effects accompanied partially by XOD activity inhibition. Therefore, the CC mixture may have potential as a treatment for hyperuricemia and gout.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 474-474
Author(s):  
Yoshiki Shimizu ◽  
Tsuyoshi Sakurada ◽  
Sayuri Matsuoka ◽  
Kei Yui ◽  
Takayuki Hosoi

Abstract Objectives This study was aimed to evaluate the effect of vine tea extract (VE) which contained ampelopsin (AMP) on postprandial serum uric acid levels. Methods A randomized, placebo controlled, and crossover study was performed from January 2018 to June 2018. The participants were Japanese male whose fasting serum uric acid levels were between 5.0 mg/dL and 7.0 mg/dL. The purine (RNA) loading test was conducted in this study. In brief, after fasting blood collection, the subjects ingested 4 g of yeast RNA and trial supplements (500 mg of VE (150 mg of AMP) or placebo), their blood and urine were subsequently collected every 1 hr for 4 hr. Uric acid and creatinine (Cr) levels in the blood and urine were measured. The primary outcome was postprandial uric acid area under the curve (AUC) and the secondary outcomes were postprandial uric acid, Cr clearance, urinary uric acid excretion, uric acid clearance, and fractional excretion of uric acid (FEUA). To investigate the urate lowering mechanism of VE, effect of VE or AMP on xanthine oxidase (XO) and urate transporter function was assessed in vitro. Results Of 119 participants screened, 36 males who met inclusion criteria were enrolled and the subjects were randomly assigned to two groups. Of these, 16 in X group and 18 in Y group were completed of the study. The values were expressed as mean ± SE. The postprandial uric acid AUC of VE (199.14 ± 62.38 mg · min/dL) was lower than that of placebo (214.41 ± 66.91 mg · min/dL), but it was not significant (P = 0.166). On the other hand, intake of VE induced the increase of urinary uric acid excretion (180 min; VE 0.58 ± 0.03 mg/kg/hr; P0.52 ± 0.03 mg/kg/hr; P = 0.044) and FEUA (180 min; VE 0.58 ± 0.03 mg/kg/hr; P 0.52 ± 0.03 mg/kg/hr; P = 0.044). These results suggest VE facilitate the uric acid excretion. An exploratory efficacy analysis was performed on 23 subjects whose eGFR values were less than 89 mL/min. As a result, the intake of VE suppressed postprandial uric acid elevation in those subjects significantly. AMP and VE inhibited the activity of XO in vitro. In addition, AMP weakly inhibited the function of OAT4, one of the urate reabsorption transporters. Conclusions These results suggested that intake of VE inhibited uric acid synthesis and facilitated of urate excretion, thereby suppression of the elevation of postprandial serum uric acid was observed. Funding Sources This study was supported by FANCL Corporation.


Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3323
Author(s):  
Yoon-Young Sung ◽  
Dong-Seon Kim

Hyperuricemia is the primary cause of gouty arthritis and other metabolic disorders. Eggshell membrane (EM) is an effective and safe supplement for curing pain and stiffness connected with osteoarthritis. However, the effect of EM on hyperuricemia is unclear. This study determines the effects of EM on potassium oxonate-injected hyperuricemia. Uric acid, creatinine, blood urea nitrogen concentrations in the serum, and xanthine oxidase activity in the liver are measured. Protein levels of renal urate transporter 1 (URAT1), organic anion transporters 1 (OAT1), glucose transporter 9 (GLUT9), and ATP-binding cassette transporter G2 (ABCG2) in the kidney are determined with renal histopathology. The results demonstrate that EM reduces serum uric acid levels and increases urine uric acid levels in hyperuricemic rats. Moreover, EM downregulates renal URAT1 protein expression, upregulates OAT1 and ABCG2, but does not change GLUT9 expression. Additionally, EM does not change xanthine oxidase activity in the liver or the serum. EM also decreases uric acid uptake into oocytes expressing hURAT1. Finally, EM markedly reduces renal inflammation and serum interleukin-1β levels. These findings suggest that EM exhibits antihyperuricemic effects by promoting renal urate excretion and regulating renal urate transporters. Therefore, EM may be useful in the prevention and treatment of gout and hyperuricemia.


Phytomedicine ◽  
2021 ◽  
Vol 80 ◽  
pp. 153374
Author(s):  
Yanyu Chen ◽  
Zean Zhao ◽  
Yongmei Li ◽  
Yang Yang ◽  
Lu Li ◽  
...  

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1328.3-1329
Author(s):  
M. Chen ◽  
X. Lu ◽  
H. Wu

Background:About 20% of individuals in the USA have asymptomatic hyperuricaemia[1]. However, Urate-lowering therapy in asymptomatic hyperuricaemia condition is still controversial considering the benefit and side effects[2]. Therefore, safe and effective anti-hyperuricemia therapies are necessary.Objectives:Bergenin, the major bioactive ingredient isolated from Saxifraga stolonifera, could activate SIRT1. In this study, we identify the effect of bergenin on hyperuricemia, and explored the related mechanisms.Methods:Significant hyperuricemia was established in C57BL/6N mice treated with oxonate and yeast polysaccharide. Bergenin was administered to the mice at the same time. The serum uric acid and creatinine levels, clearance of uric acid and creatinine, the intestinal uric acid excretion, and renal pathological lesions were determined were used to evaluate the anti-hyperuricemic effects. The location and expression levels of ABCG2 in the kidney and intestine were analyzed. HK-2 and Caco-2 cell lines were exposed to soluble uric acid with or without the treatment of Bergenin. Then the expression of ABCG2 and underlying mechanisms were explored.Results:The administration of bergenin decreased serum uric acid in hyperuricemic mice by the promotion of uric acid excretion both in kidney and intestine. Bergenin recued the downregulation of ABCG2 in the kidney of hyperuricemic mice and upregulated the expression of ABCG2 in the jejunum and ileum. In vitro, Bergenin significantly increased the expression of ABCG2 as well as activated SIRT1, which was reversed by addition of PPARg antagonist GW9662 and siPPARg.Conclusion:These findings suggest bergenin increases uric acid excretion both in the kidney and intestines, which may be related to the upregulation of ABCG2 via SIRT1- PPARg pathway.References:[1]Zhu, Y., Pandya, B. J. & Choi, H. K. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007–2008. Arthritis Rheum. 63, 3136–3141 (2011).[2]Joosten LAB, Crisan TO, Bjornstad P, Johnson RJ: Asymptomatic hyperuricaemia: a silent activator of the innate immune system. Nature reviews Rheumatology 2020, 16(2):75-86.Disclosure of Interests:None declared


1972 ◽  
Vol 15 (4) ◽  
pp. 338-346 ◽  
Author(s):  
Herbert S. Diamond ◽  
Robert Lazarus ◽  
David Kaplan ◽  
David Halberstam

1929 ◽  
Vol 23 (6) ◽  
pp. 1175-1177
Author(s):  
Kate Madders ◽  
Robert Alexander McCance

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 851.2-851
Author(s):  
Z. Zhong ◽  
Y. Huang ◽  
X. Huang ◽  
Q. Huang ◽  
Y. Liu ◽  
...  

Background:Underexcretion of uric acid is the dominant mechanism leading to hyperuricemia [1] and the 24-hour urinary uric acid excretion is an important measurement. However, it is inconvenient due to accurate timing and complete collection of the specimen.Objectives:The aim of this study was to investigate the relationship between serum uric acid to creatinine ratio (sUACR) and 24-hour urinary uric acid excretion in gout patients.Methods:A total of 110 gout patients fulfilling 2015 ACR/EULAR classification criteria from Guangdong Second Provincial General Hospital from January 2019 to January 2021 were retrospectively enrolled in this study. Patients were divided into underexcretion group (<3600 μmol/24h) and non-underexcretion group (≥3600 μmol/24h). The correlation between sUACR and 24-hour urinary uric acid excretion was analyzed by the Pearson’s correlations analysis. Receiver operation characteristic (ROC) curves were performed to assess the utility of sUACR for discriminating between underexcretion group and non-underexcretion group. Furthermore, the risk factors of uric acid underexcretion were evaluated using binary logistic regression analysis.Results:sUACR in the underexcretion group was significantly lower than the non-underexcretion group (p=0.0001). Besides, sUACR was positively correlated with 24-hour urinary uric acid excretion (r=0.4833, p<0.0001). Furthermore, ROC suggested that the area under the curve (AUC) of sUACR was 0.728, which was higher that of serum uric acid and creatinine. The optimal cutoff point of sUACR was 5.2312, with a sensitivity and specificity of 71.9% and 67.9%. Logistic analysis results revealed that decreased sUACR (<5.2312) was an independent risk factor of underexcretion of uric acid (OR =5.510, 95% CI: 1.952-15.550, P=0.001).Conclusion:sUACR is lower in gout patients with underexcretion of uric acid and may serve as a useful and convenient marker of assessing underexcretion of uric acid in gout patients.References:[1]Perez-Ruiz F, Calabozo M, Erauskin GG, Ruibal A, Herrero-Beites AM. Renal underexcretion of uric acid is present in patients with apparent high urinary uric acid output. Arthritis Rheum 2002; 47: 610–13.Figure 1.A. Comparison of serum uric acid to creatinine ratio between underexcretion group and non-underexcretion group. B. Correlation between serum uric acid to creatinine ratio and 24h uric acid excretion.Disclosure of Interests:None declared.


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