title: Polydatin ameliorates renal injury by attenuating oxidative stress-related inflammatory responses in fructose-induced urate nephropathic mice.
abstract: A series of studies have recently demonstrated that the oxidative stress, nuclear factor-kappa B (NF-κB) activation and the subsequent coordinated inflammatory responses played an important role in the pathogenesis of urate nephropathy (UN). Polydatin has been suggested to have the properties of anti-oxidative, anti-inflammatory and nephroprotective effects. However, the possible protective and beneficial effects of polydatin on UN are not fully elucidated. Therefore, we investigated the potential beneficial effects and possible mechanisms of polydatin on UN. In this study, polydatin showed inhibitory activities on xanthine oxidase to repress the level of serum uric acid in vivo and in vitro. Further investigations revealed that polydatin displayed little toxic effects and significantly ameliorated the renal function in fructose-induced UN mice. The nephroprotective activities of polydatin was not only due to the effects on remarkably attenuating the oxidative stress induced by uric acid, but also on markedly suppressing the oxidative stress-related inflammatory cascade, including decreasing the expressions of NF-κB p65, COX-2 and iNOS proteins and inhibiting the productions of TNF-α, PGE(2) and IL-1β. These findings elucidated that polydatin exhibited prominent nephroprotective activities and low toxic effects.
authors.affiliation: School of Pharmacy, South-Central University for Nationalities, Wuhan 430074, PR China. clyhappy05@163.com
authors.forename: Lvyi
authors.initials: L
authors.lastname: Chen
authors.forename: Zhou
authors.initials: Z
authors.lastname: Lan
authors.forename: Qinxiong
authors.initials: Q
authors.lastname: Lin
authors.forename: Xue
authors.initials: X
authors.lastname: Mi
authors.forename: Yingying
authors.initials: Y
authors.lastname: He
authors.forename: Liuhong
authors.initials: L
authors.lastname: Wei
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Lin
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
authors.forename: Xukun
authors.initials: X
authors.lastname: Deng
mesh_terms: D000818:Animals; D001774:Blood Chemical Analysis; D001835:Body Weight / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004195:Disease Models, Animal; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D005632:Fructose / Q000633:toxicity; D005960:Glucosides / Q000494:pharmacology*; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D007674:Kidney Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D016328:NF-kappa B / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D020011:Protective Agents / Q000494:pharmacology; D013267:Stilbenes / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014527:Uric Acid / Q000097:blood* / Q000378:metabolism; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D004365:Drugs, Chinese Herbal; D005960:Glucosides; D053583:Interleukin-1beta; D016328:NF-kappa B; D020011:Protective Agents; D013267:Stilbenes; D014409:Tumor Necrosis Factor-alpha; D014527:Uric Acid; D005632:Fructose; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D014969:Xanthine Oxidase; D015232:Dinoprostone; C058229:polydatin