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首页> 外文期刊>International journal of molecular medicine >Schisandrae semen essential oil attenuates oxidative stress-induced cell damage in C2C12 murine skeletal muscle cells through Nrf2-mediated upregulation of HO-1
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Schisandrae semen essential oil attenuates oxidative stress-induced cell damage in C2C12 murine skeletal muscle cells through Nrf2-mediated upregulation of HO-1

机译:五味子精油通过Nrf2介导的HO-1上调减轻C2C12小鼠骨骼肌细胞中氧化应激诱导的细胞损伤

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摘要

The aim of the present study was to examine the cytoprotective effects of Schisandrae semen essential oil (SSeo), purified from Schisandrae fructus, against oxidative stress-induced cell damage in C2C12 myoblasts. SSeo attenuated hydrogen peroxide (H2O2)-induced growth inhibition and exhibited scavenging activity against the intracellular reactive oxygen species (ROS) that were induced by H2O2. SSeo also inhibited comet tail formation, chromatin condensation and phospho-histone gamma H2A.X expression, suggesting that it prevents H2O2-induced cellular DNA damage and apoptotic cell death. Furthermore, SSeo significantly enhanced the expression of heme oxygenase-1 (HO-1) associated with the induction of nuclear factor erythroid-2-related factor 2 (Nrf2) in a time- and concentration-dependent manner. In addition, the protective effect of SSeo on H2O2-induced C2C12 cell damage was significantly inhibited by zinc protoporphyrin IX, an HO-1 competitive inhibitor, in C2C12 cells. These findings suggest that SSeo augments the cellular antioxidant defense capacity through intrinsic free radical scavenging activity and activation of the Nrf2/HO-1 pathway, thereby protecting the C2C12 cells from H2O2-induced oxidative cytotoxicity. As a result, SSeo may have therapeutic potential in the development of functional foods and as the raw material for medicines to protect against oxidative stress.
机译:本研究的目的是检查从五味子中提取的五味子精液(SSeo)对C2C12成肌细胞氧化应激诱导的细胞损伤的细胞保护作用。 SSeo减弱了过氧化氢(H2O2)诱导的生长抑制,并表现出对H2O2诱导的细胞内活性氧(ROS)的清除活性。 SSeo还抑制彗星尾巴的形成,染色质浓缩和磷酸化组蛋白γH2A.X的表达,这表明它可以防止H2O2诱导的细胞DNA损伤和凋亡细胞死亡。此外,SSeo以时间和浓度依赖性方式显着增强了血红素加氧酶-1(HO-1)的表达,与诱导核因子红系2相关因子2(Nrf2)相关。此外,SSeo对H2O2诱导的C2C12细胞损伤的保护作用被HO-1竞争性抑制剂原卟啉锌IX显着抑制。这些发现表明,SSeo通过固有的自由基清除活性和Nrf2 / HO-1途径的活化来增强细胞的抗氧化防御能力,从而保护C2C12细胞免受H2O2诱导的氧化细胞毒性作用。因此,SSeo可能在功能性食品的开发中以及作为抗氧化应激的药物原料具有治疗潜力。

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