痛风是一种晶体相关性关节病，由单钠尿酸沉积引起。目前，寻找适当的治疗方法和新药以降低血清尿酸水平和痛风风险是一个重要的研究领域。茶黄素是一种天然存在的化合物，具有苯二氮卓骨架的特征。茶黄素的显著益处已经得到充分的记录。近年来，已经进行了大量的研究，取得了优异的抗痛风效果。通过文献综述和网络药理学预测对茶黄素的抗痛风作用机制进行了全面分析，并总结了提高茶黄素生物利用度的策略。本综述总结了茶黄素治疗痛风的活性成分和药理学机制，并通过对茶黄素的抗痛风作用的文献综述和网络药理学，澄清了茶黄素与痛风的关系、相关成分和抗痛风作用的潜在机制。茶黄素通过下调葡萄糖转运蛋白9（GLUT9）和尿酸转运蛋白1（URAT1）的基因和蛋白质表达，同时上调有机阴离子转运蛋白1（OAT1）、有机阳离子转运蛋白N1（OCTN1）、有机阳离子转运蛋白1/2（Oct1/2）和有机阴离子转运蛋白2（OAT2）的mRNA表达水平，发挥抗痛风的作用。网络药理学预测表明，茶黄素可以通过ATP结合盒亚家族B成员1（ABCB1）、重组丝裂原激活蛋白激酶14（MAPK14）、端粒酶反转转录酶（TERT）、信号转导和转录激活因子1（STAT1）、基质金属蛋白酶2（MMP2）、B细胞淋巴瘤-2（BCL2）和基质金属蛋白酶14（MMP14）的靶点来调节AGE-RAGE和癌症信号通路，发挥抗痛风的作用。本综述提出了茶黄素的抗痛风作用机制及提高其生物利用度的策略，为抗痛风治疗措施和新型抗痛风药物的开发提供了研究策略。Copyright © 2023 Elsevier GmbH. All rights reserved.

Gout is a crystal related arthropathy caused by monosodium urate deposition. At present, the identification of appropriate treatments and new drugs to reduce serum uric acid levels and gout risk is a major research area.Theaflavins are naturally occurring compounds characterized by a benzodiazepine skeleton. The significant benefits of theaflavins have been well documented. A large number of studies have been carried out and excellent anti-gout results have been achieved in recent years.A comprehensive analysis of the mechanism of the anti-gout effect of theaflavins is presented through a literature review and network pharmacology prediction, and strategies for increasing the bioavailability of theaflavins are summarized.In this review, the active components and pharmacological mechanisms of theaflavins in the treatment of gout were summarized, and the relationship between theaflavins and gout, the relevant components, and the potential mechanisms of anti-gout action were clarified by reviewing the literature on the anti-gout effects of theaflavins and network pharmacology.Theaflavins exert anti-gout effects by down regulating the gene and protein expression of glucose transporter 9 (GLUT9) and uric acid transporter 1 (URAT1), while upregulating the mRNA expression levels of organic anion transporter 1 (OAT1), organic cation transporter N1 (OCTN1), organic cation transporters 1/2 (Oct1/2), and organic anion transporter 2 (OAT2). Network pharmacology prediction indicate that theaflavins can regulate the AGE-RAGE and cancer signaling pathways through ATP-binding cassette subfamily B member 1 (ABCB1), recombinant mitogen activated protein kinase 14 (MAPK14), telomerase reverse tranase (TERT), signal transducer and activator of transcription 1 (STAT1), matrix metalloproteinase 2 (MMP2), B-cell lymphoma-2 (BCL2), and matrix metalloproteinase 14 (MMP14) targets for anti-gout effects.This review presents the mechanisms of anti-gout action of theaflavins and strategies for improving the bioavailability of theaflavins, as well as providing research strategies for anti-gout treatment measures and the development of novel anti-gout drugs.Copyright © 2023 Elsevier GmbH. All rights reserved.