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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。
Oxidative stress is the main mechanism of alcoholic liver disease (ALD), so the antioxidant activity of the active substance has potential ALD treatment. In this study, we explored the protective effect of S-adenosylmethionine (SAM) and / or andrographolide (AD) on ethanol-induced oxidative stress injury in hepatocytes. First of all, we cultured hepatocytes L-02 in vitro. After treated with 100 mmol / L ethanol for 24 h, we found that the activity of the cells was significantly decreased, the content of intracellular reactive oxygen species (ROS) increased significantly and the accumulation of lipid accumulated. Related enzymes such as triglycerides, cholesterol, transaminases and homocysteine and other substances. However, the pretreatment with 100μmol / L SAM or (and) 30μmol / L AD before ethanol stimulation could significantly reduce the cellular oxidative stress and at the same time reduce the release of the liver-related markers. In addition, ethanol treatment also reduced SIRT1 expression and inhibited nuclear translocation, whereas treatment with SAM or (and) AD further improved SIRT1 expression and activity. The above results show that SAM or (and) AD can reduce the level of oxidative stress induced by ethanol, and the combination of the two may have a potential therapeutic effect on ALD.