Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties
Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties
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DOI：
10.1007/s00709-015-0796-3
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发表时间：
2016-01-01
期刊：
影响因子：
2.9
通讯作者：
Bolkent, Sehnaz
中科院分区：
文献类型：
--
作者：
Gezginci-Oktayoglu, Selda;Turkyilmaz, Ismet Burcu;Bolkent, Sehnaz
本研究旨在研究维生素U（vit U，S-甲基蛋氨酸）对丙戊酸（VPA）诱导的肾损伤背景下氧化应激、炎症和纤维化的影响。在本研究中，将雌性Sprague道利大鼠随机分为4组：I组由完整动物组成，II组给予vit U（50 mg/kg/天，灌胃），III组给予VPA（500 mg/kg/天，腹膜内），IV组给予VPA + vit U。在每天用VPA处理之前1小时，动物接受vit U处理，持续15天。结果表明：（1）Vit U能明显减轻肾组织病理改变，提高Na ~+/K ~+-ATP酶活性，（2）Vit U能降低肾组织中丙二醛含量和黄嘌呤氧化酶活性，提高谷胱甘肽含量、过氧化氢酶活性和超氧化物歧化酶活性，对肾损伤有保护作用。（iii）通过降低肿瘤坏死因子-α、白细胞介素-1 β、单核细胞趋化蛋白-1水平和腺苷脱氨酶活性证明了维生素U的抗炎特性;（iv）通过降低转化生长因子-β、胶原蛋白-1水平和腺苷脱氨酶活性证明了维生素U的抗纤维化作用。总的来说，这些数据表明VPA是导致肾损伤的炎症、氧化应激和纤维化的促进剂。Vit U可作为预防VPA治疗期间出现的肾损伤的潜在候选药物。
The aim of present study was to investigate the effect of vitamin U (vit U, S-methylmethionine) on oxidative stress, inflammation, and fibrosis within the context of valproic acid (VPA)-induced renal damage. In this study, female Sprague Dawley rats were randomly divided into four groups: Group I consisted of intact animals, group II was given vit U (50 mg/kg/day, by gavage), group III was given VPA (500 mg/kg/day, intraperitonally), and group IV was given VPA + vit U. The animals were treated by vit U 1 h prior to treatment with VPA every day for 15 days. The following results were obtained in vit U + VPA-treated rats: (i) the protective effect of vit U on renal damage was shown by a significant decrease in histopathological changes and an increase in Na+/K+-ATPase activity; (ii) anti-oxidant property of vit U was demonstrated by a decrease in malondialdehyde levels and xanthine oxidase activity and an increase in glutathione levels, catalase and superoxide dismutase activities; (iii) anti-inflammatory property of vit U was demonstrated by a decrease in tumor necrosis factor-alpha, interleukin-1 beta, monocyte chemoattractant protein-1 levels, and adenosine deaminase activity; (iv) anti-fibrotic effect of vit U was shown by a decrease in transforming growth factor-beta, collagen-1 levels, and arginase activity. Collectively, these data show that VPA is a promoter of inflammation, oxidative stress, and fibrosis which resulted in renal damage. Vit U can be proposed as a potential candidate for preventing renal damage which arose during the therapeutic usage of VPA.