Scope: This study established a hyperuricemic rat model to elucidate the effect of resveratrol on the transport of UA in the kidney.
Methods And Results: Hyperuricemia was induced in rats through daily oral gavage of a potassium oxonate and UA mixture over 3 weeks. Our results revealed that resveratrol significantly reduced the serum UA levels but not creatinine, c-creative protein, alanine aminotransferase, or aspartate aminotransferase levels in these rats. Furthermore, renal URAT1 and OAT1 mRNA expression were significantly higher in the rats treated with allopurinol than in those with no treatment. Therefore, allopurinol not only inhibited UA production but also mediated renal URAT1 and OAT1 expression. The correlation analysis revealed that UA levels correlated negatively with renal IL-6 mRNA expression in rats treated with allopurinol. Moreover, URAT1 showed strong immunoreactivity in the distal convoluted tubule of rats treated with allopurinol or resveratrol and in hyperuricemic treated with allopurinol. Finally, in the rats treated with resveratrol, UA levels correlated negatively with renal URAT1 mRNA expression; thus, resveratrol reduced URAT1 mRNA expression under high UA levels, thereby reducing UA reabsorption in renal cells.
Conclusion: Resveratrol contributes to URAT1 expression, which is potentially useful in therapeutic strategies aimed at treating hyperuricemia.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/mnfr.201601030 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Compound heterozygous mutations (p.L68R∗37 and p.T241N) lead to abnormal protein levels and structures in hereditary FVII deficiency.
Blood Coagul Fibrinolysis
December 2024
Department of Hematology, The Second Affiliated Hospital, Chongqing Medical University, Jiangnan, Chongqing, China.
Background: Congenital factor VII (FVII) deficiency is a genetic disorder characterized by decreased FVII activity, which sometimes leads to fatal bleeding. Numerous variants have been found in FVII deficiency, but mutations vary among patients. Each mutation deserves further exploration for each patient at risk of bleeding.
View Article and Find Full Text PDFIdentification of SETD4 as an Onco-Immunological Biomarker Encompassing the Tumor Microenvironment, Prognoses, and Therapeutic Responses in Various Human Cancers.
Immun Inflamm Dis
January 2025
Second Department of Oncology, Guangdong Second Provincial General Hospital, Guangzhou, China.
Background: SET domain-containing protein 4 (SETD4) is a histone methyltransferase that has been shown to modulate cell proliferation, differentiation, and inflammatory responses by regulating histone H4 trimethylation (H4K20me3). Previous reports have demonstrated its function in the quiescence of cancer stem cells as well as drug resistance in several cancers. A limited number of systematic studies have examined SETD4's role in the tumor microenvironment, pathogenesis, prognosis, and therapeutic response.
View Article and Find Full Text PDFEmbedding a ribonuclease in the spore crust couples gene expression to spore development in Bacillus subtilis.
Nucleic Acids Res
January 2025
EGM CNRS, Université Paris-Cité,Institut de Biologie Physico-Chimique, 13 rue Pierre et Marie Curie, 75005 Paris, France.
Faced with nutritional stress, some bacteria form endospores capable of enduring extreme conditions for long periods of time; yet the function of many proteins expressed during sporulation remains a mystery. We identify one such protein, KapD, as a 3'-exoribonuclease expressed under control of the mother cell-specific transcription factors SigE and SigK in Bacillus subtilis. KapD dynamically assembles over the spore surface through a direct interaction with the major crust protein CotY.
View Article and Find Full Text PDFKW2478 and Cisplatin Synergistically Anti-colorectal Cancer by Targeting PI3K/AKT/mTOR Pathway.
Anticancer Agents Med Chem
January 2025
Laboratory Animal Center, Affiliated Hospital of Chengde Medical University, Chengde, Hebei, 067000, P.R. China.
Objective: The objective of this study is to examine the impact of KW-2478 combined with DDP on colorectal cancer cells both in vitro and in vivo and to elucidate the molecular mechanism of KW-2478 in colorectal cancer.
Methods: qRT-PCR and Western blot were employed to assess HSP90 mRNA and protein expression in normal intestinal epithelial and colorectal cancer cells. DLD-1 and HCT116 were selected for the experiment.
Mizagliflozin ameliorates diabetes induced kidney injury by inhibitor inhibit inflammation and oxidative stress.
World J Diabetes
January 2025
Department of Nephrology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.
Background: Mizagliflozin (MIZ) is a specific inhibitor of sodium-glucose cotransport protein 1 (SGLT1) originally developed as a medication for diabetes.
Aim: To explore the impact of MIZ on diabetic nephropathy (DN).
Methods: Diabetic mice were created using db/db mice.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!