穿心莲内酯联合S-腺苷甲硫氨酸抑制乙醇诱导肝细胞氧化应激损伤

发布时间：2018-04-24 10:40

本文选题：S-腺苷甲硫氨酸 + 穿心莲内酯　；参考：《基因组学与应用生物学》2017年07期

【摘要】：氧化应激是酒精性肝病(ALD)发生的主要机制,因此具有抗氧化作用的活性物质对ALD具有潜在的治疗意义。在本研究当中,我们探讨了S-腺苷甲硫氨酸(SAM)和(或)穿心莲内酯(AD)对乙醇诱导肝细胞氧化应激损伤的保护作用。首先我们体外培养肝细胞L-02,用100 mmol/L乙醇作用24 h后发现,细胞的活性明显降低,胞内活性氧(ROS)含量显著增多以及脂质蓄积,同时细胞释放多种与肝病相关酶类如甘油三脂、胆固醇、转氨酶以及同型半胱氨酸等物质。而乙醇刺激前采用100μmol/L SAM或(和)30μmol/L AD处理细胞后,可明显降低细胞的氧化应激水平,同时能减少上述肝病相关标志物的的释放。此外,乙醇处理也可降低细胞内去乙酰化酶SIRT1的表达并抑制其核转位,而采用SAM或(和)AD处理后可进一步改善SIRT1的表达及活性。以上结果表明SAM或(和)AD能降低乙醇所致的氧化应激水平,两者联合应用可能对ALD具有潜在的治疗效果。
[Abstract]:Oxidative stress is the main mechanism of ALD, so the active substance with antioxidant activity has potential therapeutic significance for ALD. In this study, we investigated the protective effects of S-adenosine methionine (SAM) and / or andrographolide (ADD) on ethanol induced oxidative stress injury in hepatocytes. First, we cultured L-02 hepatocytes in vitro, and after treated with 100 mmol/L ethanol for 24 h, we found that the activity of the cells decreased significantly, the intracellular reactive oxygen species (Ros) content increased and lipid accumulation was significantly increased, and the cells released many enzymes related to liver diseases, such as triglyceride. Cholesterol, transaminase and homocysteine. However, after treated with 100 渭 mol/L SAM or (and 30 渭 mol/L AD) before ethanol stimulation, the oxidative stress level of the cells was significantly decreased and the release of the above-mentioned markers of liver disease was decreased. In addition, ethanol treatment also decreased the expression of deacetylase SIRT1 and inhibited its nuclear translocation, while SAM or / and AD could further improve the expression and activity of SIRT1. These results suggest that SAM or / and AD can reduce the level of oxidative stress induced by ethanol, and the combination of the two may have potential therapeutic effect on ALD.
【作者单位】：南华大学附属第二医院急诊内科;南华大学附属第一医院急诊科;南华大学附属第二医院超声医学科;
【基金】：湖南省卫生计生委科研基金(B2016136) 湖南省分子靶标新药研究协同创新中心资助项目(湘教通2015351)共同资助
【分类号】：R575

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