The anti-hyperuricemic effects of green alga Enteromorpha prolifera polysaccharide via regulation of the uric acid transporters in vivo

2021 ◽  
pp. 112630
Author(s):  
Xiaoqing Li ◽  
Xiaoxiang Gao ◽  
Hui Zhang ◽  
Yuanyuan Liu ◽  
Md Moklesur Rahman Sarker ◽  
...  
Keyword(s):  
Uric Acid ◽  
Green Alga ◽  
Enteromorpha Prolifera ◽  
Uric Acid Transporters

Regulation of Catechins in Uric Acid Metabolism Disorder Related Human Diseases

2020 ◽  
Vol 20 (18) ◽  
pp. 1857-1866
Author(s):  
Dan Wu ◽  
Wenji Zhang ◽  
Xingfei Lai ◽  
Qiuhua Li ◽  
Lingli Sun ◽  
...  
Keyword(s):  
Uric Acid ◽  
Acid Metabolism ◽  
Inflammatory Reactions ◽  
Metabolism Disorder ◽  
Uric Acid Transporters ◽  
Uric Acid Secretion ◽  
High Uric Acid ◽  
Urate Crystals

Uric acid is the end product of purine metabolism in humans. High uric acid levels form sodium urate crystals that trigger biological processes, which lead to the development of several diseases, including diabetes, hyperuricemia, gout, inflammatory disease, kidney disease, cardiovascular disease and hypertension. Catechins have been suggested to be beneficial for the regulation of uric acid metabolic disorders due to their powerful antioxidant and anti-inflammatory properties. To identify an effective and safe natural substance that can decrease levels of serum uric acid to improve uric acid metabolism disorders. A search was performed on PubMed, Web of Science and Google Scholar to identify comprehensive studies that presented summarized data on the use of catechins in lowering uric acid levels in diseases. This review details the role of catechins in inhibiting the activity of xanthine oxidase to decrease uric acid overproduction in the liver and in regulating expressions of uric acid transporters, URAT1, OAT1, OAT3, ABCG2 and GLUT9, to balance levels of uric acid secretion and reabsorption through the kidney and intestine. Additionally, Catechins were also found to prevent monosodium urate-induced inflammatory reactions. In vivo, catechins can be used to decrease high uric acid levels that result from hyperuricemia and related diseases. Catechins can be used to maintain the balance of uric acid metabolism.

scholarly journals In vivo identification of uric acid stones with dual-energy CT: diagnostic performance evaluation in patients

2009 ◽  
Vol 35 (5) ◽  
pp. 629-635 ◽  
Author(s):  
Paul Stolzmann ◽  
Marko Kozomara ◽  
Natalie Chuck ◽  
Michael Müntener ◽  
Sebastian Leschka ◽  
...  
Keyword(s):  
Uric Acid ◽  
Performance Evaluation ◽  
Diagnostic Performance ◽  
Dual Energy ◽  
Dual Energy Ct ◽  
Uric Acid Stones

Bmk9 and Uricase Nanoparticle Complex for the Treatment of Gouty Arthritis and Uric Acid Nephropathy

2021 ◽  
Vol 17 (10) ◽  
pp. 2071-2084
Author(s):  
Tianjiao Han ◽  
Meiying Wang ◽  
Wenchao Li ◽  
Mingxing An ◽  
Hongzheng Fu
Keyword(s):  
Uric Acid ◽  
Drug Loading ◽  
Gouty Arthritis ◽  
The Body ◽  
Key Points ◽  
Uric Acid Nephropathy ◽  
Charged Carrier ◽  
Dual Drug

Uric acid is the final product of purine metabolism, and excessive serum uric acid can cause gouty arthritis and uric acid nephropathy. Therefore, lowering the uric acid level and alleviating inflammation in the body are the key points to treating these diseases. A stable nanosuspension of peptide BmK9 was prepared by the precipitation-ultrasonication method. By combining uricase on the surface of a positively charged carrier, a complex consisting of neutral rod-shaped BmK9 and uricase nanoparticles (Nplex) was formed to achieve the delivery of BmK9 and uricase, respectively. The formulation of Nplex has a diameter of 180 nm and drug loading up to 200%, which releases BmK9 and uricase slowly and steadily in drug release tests in vitro. There was significantly improved pharmacokinetic behavior of the two drugs because Nplex prolonged the half-life and increased tissue accumulation. Histological assessments showed that the dual drug Nplex can reduce the inflammation response in acute gouty arthritis and chronic uric acid nephropathy in vivo. In the macrophage system, there was lower toxicity and increased beneficial effect on inflammation with Nplex than free BmK9 or uricase. Collectively, this novel formulation provides a dual drug delivery system that can treat gouty arthritis and uric acid nephropathy.

scholarly journals Concentration-Dependent Inhibitory Effect of Irbesartan on Renal Uric Acid Transporters

2010 ◽  
Vol 114 (1) ◽  
pp. 115-118 ◽  
Author(s):  
Makiko Nakamura ◽  
Naohiko Anzai ◽  
Promsuk Jutabha ◽  
Hiroyuki Sato ◽  
Hiroyuki Sakurai ◽  
...  
Keyword(s):  
Uric Acid ◽  
Inhibitory Effect ◽  
Uric Acid Transporters

scholarly journals Human URAT1/SLC22A12 gene promoter is regulated by 27-hydroxycholesterol through estrogen response elements

2019 ◽  
Author(s):  
Masaya Matsubayashi ◽  
Yoshihiko M. Sakaguchi ◽  
Yoshiki Sahara ◽  
Hitoki Nanaura ◽  
Sotaro Kikuchi ◽  
...  
Keyword(s):  
Uric Acid ◽  
Serum Uric Acid ◽  
Cholesterol Metabolism ◽  
Gene Promoter ◽  
Human Kidney ◽  
Response Elements ◽  
Estrogen Response ◽  
Uric Acid Transporters ◽  
Estrogen Response Elements ◽  
Phylogenic Relationship

AbstractElevated levels of uric acid, a metabolite of purine in humans, is related to various diseases, such as gout, atherosclerosis and renal dysfunction. The excretion and reabsorption of uric acid to/from urine is tightly regulated by uric acid transporters. The amino acid sequences of uric acid reabsorption transporters, URAT1/SLC22A12, OAT4/SLC22A11, and OAT10/SLC22A13, share closer phylogenic relationship, whereas the gene promoter sequences are distant phylogenic relationship. Through the single-cell RNA-sequencing analysis of an adult human kidney, we found that only a small number of cells express these transporters, despite their role in the regulation of serum uric acid levels. Transcriptional motif analysis on these transporter genes, revealed that the URAT1/SLC22A12 gene promoter displayed the most conserved estrogen response elements (EREs) among the three transporters. The endogenous selective estrogen receptor modulator (SERM) 27-hydroxycholesterol (27HC) had positive effects on the transcriptional activity of URAT1/SLC22A12. We also found that 27HC increased the protein and gene expression of URAT1/SLC22A12 in mouse kidneys and human kidney organoids, respectively. These results strongly suggest the role of 27HC for URAT1/SLC22A12 expression in renal proximal tubules and upregulation of serum uric acid levels and also show the relationship between cholesterol metabolism and serum uric acid regulation.Significance StatementThe elevated levels of serum uric acid cause various diseases, and the excretion/reabsorption of uric acid to/from urine is tightly regulated by the uric acid transporters. We found that despite the role in serum uric acid regulation, only a small number of cells express URAT1/SLC22A12. We also found that URAT1/SLC22A12 gene promoter region has effective estrogen response elements, and endogenous selective estrogen receptor (ER) modulator 27-hydroxycholesterol (27HC) increased URAT1/SLC22A12 expression in the mice kidneys and human kidney organoids. These suggest that 27HC increases URAT1/SLC22A12 expression and upregulate serum uric acid levels. Since 27HC connects cholesterol metabolism, our study indicates the important link between cholesterol metabolism and serum uric acid regulation, and also provides a novel therapeutic approach to hyperuricemia.

scholarly journals A taxonomically-restricted Uric Acid transporter provides insight into antioxidant equilibrium

2018 ◽  
Author(s):  
Diogo Oliveira ◽  
André Machado ◽  
Tiago Cardoso ◽  
Mónica Lopes-Marques ◽  
L. Filipe C. Castro ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Uric Acid ◽  
Seminal Fluid ◽  
Urogenital System ◽  
The Novel ◽  
Morphological Adaptations ◽  
Gene Expression Quantification ◽  
Uric Acid Transporters ◽  
Clawed Frog

AbstractNucleobase-Ascorbate Transporter (NAT) family includes ascorbic acid, nucleobases and uric acid transporters, with a broad evolutionary distribution. In vertebrates, four members have been previously recognized, the ascorbate transporters Slc23a1 and Slc3a2, the nucleobase transporter Slc23a4 and an orphan transporter SLC23A3. Here we identify a fifth member of the vertebrateslc23complement (slc23a5), expressed in neopterygians (gars and teleosts) and amphibians, and clarify the evolutionary relationships between the novel gene and knownslc23genes. Further comparative analysis puts forward uric acid as the preferred substrate for Slc23a5. Gene expression quantification suggests kidney and testis as major expression sites inXenopus tropicalis(western clawed frog) andDanio rerio(zebrafish). Additional expression in brain was detected inD. rerio, while in the NeoteleosteiOryzias latipes(medaka)slc23a5expression is restricted to brain. The biological relevance of the retention of an extra transporter in fish and amphibians is examined: with respect to the (1) antioxidant role of uric and ascorbic acid in seminal fluid and brain, (2) the ability to endogenously synthesize ascorbic acid and (3) the morphological adaptations of the male urogenital system.

Effects of some anti-inflammatory drugs on 12 blood constituents: protocol for the study of in vivo effects of drugs.

1985 ◽  
Vol 31 (7) ◽  
pp. 1141-1143 ◽  
Author(s):  
Z Jelić-Ivanović ◽  
S Spasić ◽  
N Majkić-Singh ◽  
P Todorović
Keyword(s):  
Uric Acid ◽  
Acetylsalicylic Acid ◽  
Total Protein ◽  
Inorganic Phosphate ◽  
Drug Effects ◽  
Urea Nitrogen ◽  
Blood Constituents ◽  
Inflammatory Drugs ◽  
In Vivo Effects

Abstract We investigated the in vivo effects of acetylsalicylic acid, diclofenac, indomethacin, ibuprofen, and ketoprofen on the concentrations of various blood constituents. Total protein, glucose, calcium, and inorganic phosphate were not significantly affected by any of these drugs. Ketoprofen had no definite influence on any constituent. Acetylsalicylic acid induced an increase in cholesterol, triglyceride, and iron; albumin, uric acid, and creatinine decreased with ibuprofen therapy. Urea nitrogen increased in patients treated with diclofenac or indomethacin. Our protocol for the study of in vivo drug effects is discussed.

Sign in / Sign up

Export Citation Format

Share Document