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首页> 外文期刊>BMC Complementary and Alternative Medicine >Protective activity of Panduratin A against Thioacetamide-induced oxidative damage: demonstration with in vitro experiments using WRL-68 liver cell line
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Protective activity of Panduratin A against Thioacetamide-induced oxidative damage: demonstration with in vitro experiments using WRL-68 liver cell line

机译:Panduratin A对硫代乙酰胺诱导的氧化损伤的保护活性:使用WRL-68肝细胞系的体外实验证明

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Background Chalcone Panduratin A (PA) has been known for its antioxidant property, but its merits against oxidative damage in liver cells has yet to be investigated. Hence, the paper aimed at accomplishing this task with normal embryonic cell line WRL-68. Methods PA was isolated from Boesenbergia rotunda rhizomes and its 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging and ferric reducing power (FRAP) activities were measured in comparison with that of the standard reference drug Silymarin (SI). Oxidative damage was induced by treating the cells with 0.04 g/ml of toxic thioacetamide for 60 minutes followed by treatment with 1, 10 and 100 μg/ml concentrations of either PA or SI. The severities of oxidative stress in the control and experimental groups of cells were measured by Malondialdehyde (MDA) levels, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities. Results PA exhibited an acceptable DPPH scavenging and FRAP activities close to that of Silymarin. Treating the injured cells with PA significantly reduced the MDA level and increased the cell viability, comparable to SI. The activities of SOD, CAT and GPx were significantly elevated in the PA-treated cells in a dose dependent manner and again similar to SI. Conclusion Collectively, data suggested that PA has capacity to protect normal liver cells from oxidative damage, most likely via its antioxidant scavenging ability.
机译:背景查尔酮泛素A(PA)因其抗氧化特性而闻名,但其抗肝细胞氧化损伤的优点尚未得到研究。因此,该论文旨在用正常的胚胎细胞系WRL-68完成此任务。方法从圆形的波黑虫根茎中分离出PA,并与标准参比药物Silymarin(SI)进行比较,测定其2,2-二苯基-1-吡啶并肼基(DPPH)的清除和铁还原能力(FRAP)活性。通过用0.04 g / ml的有毒硫代乙酰胺处理细胞60分钟,然后用1、10和100μg/ ml的PA或SI浓度处理来诱导氧化损伤。通过丙二醛(MDA)水平,超氧化物歧化酶(SOD),过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)活性来测量对照组和实验组细胞的氧化应激程度。结果PA表现出可接受的DPPH清除和FRAP活性,接近于水飞蓟素。与SI相比,用PA处理受损细胞可显着降低MDA水平并提高细胞活力。在PA处理的细胞中,SOD,CAT和GPx的活性以剂量依赖性方式显着提高,再次类似于SI。结论总体而言,数据表明PA具有保护正常肝细胞免受氧化损伤的能力,这很可能是通过其抗氧化清除能力来实现的。

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