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首页> 外文期刊>Advances in Experimental Medicine and Biology >Cytoprotective Effects of an Aqueous Extracts from Atrina Pectinate Meat in H2O2-Induced Oxidative Stress in a Human Hepatocyte
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Cytoprotective Effects of an Aqueous Extracts from Atrina Pectinate Meat in H2O2-Induced Oxidative Stress in a Human Hepatocyte

机译:亚毒素含有含水提取物的细胞保护作用在人肝细胞中H2O2诱导的H2O2诱导的氧化胁迫下

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摘要

In the present study, we investigated the antioxidant activity of an aqueous extract from Atrina pectinate meat (APW) against H2O2-induced oxidative stress in a human hepatocyte. The extraction yield of APW was 30.01 +/- 0.83% and which contained the highest taurine content among free amino acid contents. APW led to the high antioxidant activity showing 2,2-azino-bis(3-ethylbenzthiazoline)6-sulfonic acid (ABTS) radical scavenging activity, good reducing power and -oxygen radical absorbance capacity (ORAC) value. Also, the results showed that APW improved the cell viability decreased by H2O2 stimulation as well as the reduction of intracellular reactive oxygen species (ROS) generation in hepatocytes. Additionally, APW up-regulated the production of antioxidant mechanisms related enzymes such as catalase and superoxide dismutase (SOD), compared to the only H2O2-treated hepatocytes. Moreover, APW increased the expressions of nuclear Nrf2 and cytosolic HO-1 in H2O2-treated hepatocytes. Interestingly, the treatment of ZnPP, a HO-1 inhibitor abolished the cell viability and intracellular ROS generation induced by APW treatment. In conclusion, this study suggests that APW protects H2O2 induced oxidative stress via up-regulating of Nrf2/HO-1 signal pathway in hepatocytes.
机译:在本研究中,我们研究了从艾里林果胶(APW)的抗氧化活性以免受人肝细胞中的H2O2诱导的氧化胁迫。 APW的提取产率为30.01 +/- 0.83%,其中包含自由氨基酸含量的最高牛磺酸含量。 APW导致高抗氧化活性,显示2,2-氮杂-BIS(3-乙基苯并噻唑啉)6-磺酸(ABTS)自由基清除活性,良好的降低功率和 - 自由基吸光度(ORAC)值。而且,结果表明,APW改善了细胞活力通过H2O2刺激降低,以及降低肝细胞中的细胞内反应性氧物质(ROS)产生。另外,与唯一的H2O2处理的肝细胞相比,APW上调了抗氧化机制的相关酶如过氧化氢酶和超氧化物歧化酶(SOD)。此外,APW在H2O2处理的肝细胞中增加了核NRF2和细胞溶质HO-1的表达。有趣的是,ZnPP的治疗,HO-1抑制剂废除了APW治疗诱导的细胞活力和细胞内ROS产生。总之,该研究表明,APW通过在肝细胞中的NRF2 / HO-1信号途径上调节NRF2 / HO-1信号途径来保护H2O2诱导的氧化应激。

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