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首页> 外文期刊>Cellular Physiology and Biochemistry >Modulation of Oxidative Stress by 17 ?2-Estradiol and Genistein in Human Hepatic Cell Lines In Vitro
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Modulation of Oxidative Stress by 17 ?2-Estradiol and Genistein in Human Hepatic Cell Lines In Vitro

机译：17α2-雌二醇和染料木黄酮对人肝细胞系体外氧化应激的调节

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>Background/Aims: estrogens and phytoestrogens exert hepatoprotection through mechanisms not clearly examined yet. Here, we investigated the protective effects exerted by 17?2-estradiol and genistein against oxidative stress in hepatocytes and hepatic stellate cells (HSCs) and the involvement of specific receptors and the intracellular signalling. Methods: Huh7.5 and LX-2, alone or in co-culture with Huh7.5, were treated with 17?2-estradiol and genistein alone or in the presence of menadione and of estrogen receptors (ERs) and G protein-coupled-estrogenic-receptors (GPER) blockers. Cell viability, mitochondrial membrane potential and oxidant/antioxidant system were measured by specific kits. Western Blot was used for the analysis of Akt and p38-mitogen-activated-protein kinases (MAPK) activation and ?±-smooth-muscle actin expression. Results: In Huh7.5, 17?2-estradiol and genistein prevented the effects of peroxidation by modulating Akt and p38MAPK activation. Similar antioxidant and protective findings were obtained in LX-2 of co-culture experiments, only. ERs and GPER blockers were able to prevent the effects of 17?2-estradiol and genistein. Conclusion: In Huh7.5 and LX-2, 17?2-estradiol and genistein counteract the effects of peroxidation through the involvement of ERs and GPER and by an intracellular signalling related to Akt and p38MAPK. As concerning LX-2, paracrine factors released by Huh7.5 play a key role in protection against oxidative stress.
机译：> 背景/目的： 雌激素和植物雌激素通过尚不清楚的机制发挥肝脏保护作用。在这里，我们研究了17β2-雌二醇和染料木黄酮对肝细胞和肝星状细胞（HSCs）氧化应激以及特定受体的参与和细胞内信号传导的保护作用。 方法： 将Huh7.5和LX-2单独或与Huh7.5共培养，分别或在存在下分别用17？2-雌二醇和染料木黄酮处理甲萘醌和雌激素受体（ER）和G蛋白偶联雌激素受体（GPER）阻滞剂的使用。细胞活力，线粒体膜电位和氧化剂/抗氧化剂系统通过特定试剂盒测量。 Western Blot用于分析Akt和p38丝裂原活化蛋白激酶（MAPK）的活化和α±平滑肌肌动蛋白的表达。 结果： 在Huh7.5中，17β2-雌二醇和染料木黄酮可通过调节Akt和p38MAPK激活来阻止过氧化作用。仅在共培养实验的LX-2中获得了类似的抗氧化剂和保护性发现。 ER和GPER阻滞剂能够预防17β2-雌二醇和染料木黄酮的作用。 结论： 在Huh7.5和LX-2中，17α2-雌二醇和染料木黄酮可通过ER和GPER的参与以及细胞内信号传导相关的作用来抵消过氧化作用。 Akt和p38MAPK。关于LX-2，Huh7.5释放的旁分泌因子在抵抗氧化应激中起关键作用。

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