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首页> 外文期刊>Archives of pharmacal research >The cytoprotective effect of Rumex Aquaticus Herba extract against hydrogen peroxide-induced oxidative stress in AGS cells
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The cytoprotective effect of Rumex Aquaticus Herba extract against hydrogen peroxide-induced oxidative stress in AGS cells

机译:Rumex Aquaticus Herba提取物抵抗过氧化氢诱导的AGS细胞氧化胁迫的细胞保护作用

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The Rumex Aquaticus Herba extract containing quercetin-3-beta-D-glucuronopyranoside (ECQ) has been reported to exhibit various pharmacological activities, including anti-inflammatory and anti-oxidative effects. This plant has been traditionally used for the treatment of diarrhea, disinfestation, edema and jaundice, and as an antipyretic drug. The aim of the present study was to investigate the ability of ECQ to protect against oxidative damage and to determine its signaling mechanism in AGS cells. The protein expressions of heme oxygenase-1 (HO-1) and nuclear factor-erythroid 2 related factor 2 (Nrf2) were measured by Western blots. Cell viability was measured by MTT assay. Intracellular reactive oxygen species (ROS) levels were measured using 2',7'-dichlorofluorescein diacetate. Glutathione peroxidase levels were measured using kits. The protein expressions of HO-1 and its upstream mediator, Nrf2, increased after ECQ treatment. The HO-1 inhibitor, ZnPP, repressed the protective effect of ECQ on H2O2-induced cell damage. We found that LY294002, a specific PI3 K/Akt inhibitor, suppressed ECQ-induced HO-1 expression. ECQ significantly attenuated H2O2-induced cytotoxicity and ROS generation. Also, ECQ enhanced the antioxidant enzyme activities of glutathione peroxidase. These results suggest that ECQ exerts a cytoprotective effect against H2O2-induced oxidative stress by upregulation of Nrf2/HO-1 via the PI3 K/Akt pathway.
机译:据报道,含有槲皮素-3-Beta-D-葡糖尿嘧啶(ecq)的Rumex Aquaticus Herba提取物,表现出各种药理活动,包括抗炎和抗氧化作用。该植物传统上用于治疗腹泻,消毒,水肿和黄疸以及作为一种解热药物。本研究的目的是探讨ECQ防止氧化损伤的能力,并确定其在AGS细胞中的信号机制。通过蛋白质印迹测量血红素氧酶-1(HO-1)和核因子 - 红细胞2相关因子2(NRF2)的蛋白表达。通过MTT测定法测量细胞活力。使用2',7'-二氯荧光蛋白测量细胞内反应性氧物质(ROS)水平。使用试剂盒测量谷胱甘肽过氧化物酶水平。 eCQ处理后HO-1及其上游介体NRF2的蛋白质表达增加。 HO-1抑制剂,ZnPP,压抑ECQ对H2O2诱导的细胞损伤的保护作用。我们发现LY294002,特定的PI3 K / AKT抑制剂,抑制ECQ诱导的HO-1表达。 ECQ显着减弱了H2O2诱导的细胞毒性和ROS生成。此外,eCQ增强了谷胱甘肽过氧化物酶的抗氧化酶活性。这些结果表明ECQ通过PI3 K / AKT途径上调NRF2 / HO-1来施加细胞保护作用对H 2 O 2诱导的氧化应激。

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