ArticleJournal of natural medicines2023
Eurycoma longifolia alkaloid components ameliorate hyperuricemic nephropathy via regulating serum uric acid level and relieving inflammatory reaction.
Article in Journal of natural medicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Therapeutic potential and pharmacological mechanisms of Traditional Chinese Medicine in gout treatment.Acta pharmacologica Sinica · 2025Review
- Inhibition of METTL3 Attenuates Renal Fibrosis by Upregulating ABCG2 m6A Modifications via IGF2BP2-Dependent Mechanisms in Hyperuricemic Nephropathy.Journal of cellular and molecular medicine · 2025Article
- Association between the serum uric acid/serum creatinine ratio and cognitive function in older adults: NHANES in the United States.Scientific reports · 2024Article
- Evaluation of comparative chemical profiling and bioactivities of medicinal and non-medicinal parts ofHeliyon · 2024Article
- Article
- Understanding Hyperuricemia: Pathogenesis, Potential Therapeutic Role of Bioactive Peptides, and Assessing Bioactive Peptide Advantages and Challenges.Foods (Basel, Switzerland) · 2023Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Hyperuricemia is an independent risk factor for chronic kidney disease. We have previously showed the uric-acid-lowering effect of Eurycoma longifolia Jack, yet the renal protective effect and mechanism of E. longifolia remain obscure. The mouse model of hyperuricemic nephropathy was induced by adenine combined with potassium oxonate in male C57BL/6 J mice. E. Longifolia alkaloid components could reduce the level of serum uric acid by regulating the expression of hepatic phosphoribosyl pyrophosphate synthase (PRPS), hypoxanthine-guanine phosphoribosyl transferase (HPRT), and renal urate transporter organic anion transporter 1 (OAT1) and ATP-binding box subfamily G member 2 (ABCG2) in HN mice. Additionally, E. Longifolia alkaloid components alleviated renal injury and function caused by hyperuricemia, which was characterized by improving renal histopathology, reducing urea nitrogen and creatinine levels. E. Longifolia alkaloid components treatment could reduce the secretion of pro-inflammatory factors by inhibiting the activation of NF-κB and NLRP3 inflammatory signaling pathways, including tumor necrosis factor α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), interleukin-1 β (IL-1β), and regulated activated normal T cell expression and secretion proteins (RANTES). Meanwhile, E. longifolia alkaloid components improved renal fibrosis, inhibited the transformation of calcium-dependent cell adhesion molecule E (E-cadherin) to α-smooth muscle actin (α-SMA) transformation, and decreased collagen 1 expression in HN mice.
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