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Green coffee hydroxycinnamic acids but not caffeine protect human HepG2 cells against oxidative stress

机译:绿色咖啡羟基肉桂酸而非咖啡因可保护人类HepG2细胞免受氧化应激

摘要

The intake of green coffee has been associated with a lower risk of diseases of oxidative etiology probably due to its high phenolic content. The present study investigated the effect of treating human HepG2 cells with different concentrations of a green coffee bean extract (GCBE) and its main hydroxycinnamic acids, 5-caffeoylquinic acid (5-CQA) and 3,5-dicaffeoylquinic acid (3,5-DCQA), and the methylxanthine caffeine (CAF), directly or prior to inducing an oxidative stress by incubating cells with 400. μM tert-butylhydroperoxide (t-BOOH). Direct treatment with GCBE (1-50. μg/mL), 5-CQA and 3,5-DCQA (1-40. μM) significantly decreased reactive oxygen species (ROS) production by HepG2 cells. Pre-treatment with GCBE, 5-CQA and 3,5-DCQA for 20. h prevented the cellular and macromolecular damage induced by t-BOOH, returning glutathione levels and the activity of antioxidant enzymes to values similar to control cells. Moreover, the increased ROS generation induced by t-BOOH was dose-dependently prevented when cells were pre-treated with GCBE, 5-CQA and 3,5-DCQA. CAF showed no protective effect. It can be concluded that GCBE and its main polyphenols, 5-CQA and 3,5-DCQA, but not caffeine, confer a significant protection against oxidative stress in vitro. © 2014 Elsevier Ltd.
机译:摄入生咖啡可能由于其高酚含量而具有较低的氧化病因疾病风险。本研究调查了用不同浓度的生咖啡豆提取物(GCBE)及其主要羟基肉桂酸,5-咖啡酰奎尼酸(5-CQA)和3,5-二咖啡酰奎尼酸(3,5- DCQA)和甲基黄嘌呤咖啡因(CAF),直接或在通过将细胞与400.μM叔丁基过氧化氢(t-BOOH)孵育而诱导氧化应激之前。用GCBE(1-50。μg/ mL),5-CQA和3,5-DCQA(1-40.μM)直接处理可显着降低HepG2细胞产生的活性氧(ROS)。用GCBE,5-CQA和3,5-DCQA预处理20 h可以防止t-BOOH引起的细胞和大分子损伤,使谷胱甘肽水平和抗氧化酶活性恢复到与对照细胞相似的水平。此外,当细胞用GCBE,5-CQA和3,5-DCQA预处理时,剂量依赖性地防止了t-BOOH诱导的ROS生成增加。 CAF无保护作用。可以得出结论,GCBE及其主要多酚5-CQA和3,5-DCQA而非咖啡因在体外具有显着的抗氧化应激保护作用。 ©2014爱思唯尔有限公司。

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