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首页> 外文期刊>The Journal of Nutritional Biochemistry >Resveratrol up-regulates SIRT1 and inhibits cellular oxidative stress in the diabetic milieu: mechanistic insights.
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Resveratrol up-regulates SIRT1 and inhibits cellular oxidative stress in the diabetic milieu: mechanistic insights.

机译：白藜芦醇可上调SIRT1并抑制糖尿病环境中的细胞氧化应激：机理研究。

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Several lines of evidence support a role for oxidative stress in diabetic complications. Diabetic patients have increased O2-- production in monocytes. Loss of SIRT1 activity may be associated with metabolic diseases such as diabetes. Several studies have shown that SIRT1 can regulate mammalian FOXO transcription factors through direct binding and/or deacetylation. However, interactions between SIRT1 and FOXO under diabetic conditions are unclear. The phytochemical resveratrol has recently gained attention for its protection against metabolic disease. Resveratrol has been shown to increase mitochondrial function by activating SIRT1. In this study, we tested the protective effect of resveratrol on cellular oxidative stress through the SIRT1-FOXO pathway under high-glucose conditions. Human monocytic (THP-1) cells were cultured in the presence of mannitol (osmolar control) or normoglycemic (NG, 5.5 mmol/l glucose) or hyperglycemic (HG, 25 mmol/l glucose) conditions in absence or presence of resveratrol (3 and 6 mumol/l) for 48 h. We first examined SIRT1 activity and oxidative stress in monocytes of Type 1 diabetes mellitus (T1DM) patients compared with healthy controls. In T1DM patients, monocytic SIRT1 expression was significantly decreased and p47phox expression was increased compared with controls. Under HG in vitro, SIRT1 and FOXO3a were significantly decreased compared with NG, and this was reversed by resveratrol treatment, concomitant with reduction in HG-induced superoxide production and p47phox. Under HG, SIRT1 small interfering RNA (siRNA) inhibited FOXO3a, and there was no beneficial effect of resveratrol in siRNA-treated HG-induced cells. Thus, resveratrol decreases HG-induced superoxide production via up-regulation of SIRT1, induction of FOXO3a and inhibition of p47phox in monocytes
机译：有几条证据支持氧化应激在糖尿病并发症中的作用。糖尿病患者单核细胞中O 2 -产生增加。 SIRT1活性的丧失可能与诸如糖尿病的代谢性疾病有关。多项研究表明，SIRT1可通过直接结合和/或脱乙酰作用来调节哺乳动物FOXO转录因子。但是，尚不清楚在糖尿病条件下SIRT1和FOXO之间的相互作用。植物化学白藜芦醇最近由于其针对代谢疾病的保护而受到关注。已显示白藜芦醇可通过激活SIRT1增强线粒体功能。在这项研究中，我们测试了白藜芦醇在高葡萄糖条件下通过SIRT1-FOXO途径对细胞氧化应激的保护作用。在不存在或存在白藜芦醇的情况下，在甘露醇（渗透压对照）或正常血糖（NG，5.5 mmol / l葡萄糖）或高血糖（HG，25 mmol / l葡萄糖）的条件下培养人单核细胞（THP-1）（3和6μmol/ l）持续48小时。我们首先检查了与健康对照组相比1型糖尿病（T1DM）患者单核细胞中SIRT1的活性和氧化应激。在T1DM患者中，单核细胞SIRT1表达与对照组相比明显降低，而p47phox表达则升高。在HG体外，与NG相比，SIRT1和FOXO3a显着降低，白藜芦醇处理可逆转SIRT1和FOXO3a，同时减少HG诱导的超氧化物和p47phox。在HG下，SIRT1小干扰RNA（siRNA）抑制了FOXO3a，白藜芦醇在siRNA处理的HG诱导的细胞中没有有益作用。因此，白藜芦醇通过上调SIRT1，诱导FOXO3a并抑制单核细胞中p47phox来降低HG诱导的超氧化物生成

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