Effect of coffee Melanoidin on human hepatoma HepG2 cells. Protection against oxidative stress induced by tert-butylhydroperoxide
Effect of coffee Melanoidin on human hepatoma HepG2 cells. Protection against oxidative stress induced by tert-butylhydroperoxide
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DOI：
10.1002/mnfr.200600228
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发表时间：
2007-05-01
影响因子：
5.2
通讯作者：
Morales, Francisco J.
中科院分区：
文献类型：
--
作者：
Goya, Luis;Delgado-Andrade, Cristina;Morales, Francisco J.
通过超滤分离咖啡汁中的可溶性高分子量组分(黑素)，然后模拟胃和胰腺的消化条件对其进行消化，并对其进行了CZE、凝胶过滤和褐变的部分表征。本研究旨在探讨咖啡黑素对叔丁基氢过氧化氢(t-BOOH)诱导的人肝癌细胞株HepG2细胞存活率(乳酸脱氢酶漏出)和氧化还原状态的潜在保护作用。以还原型谷胱甘肽(GSH)和丙二醛(MDA)浓度、活性氧(ROS)生成及抗氧化酶谷胱甘肽过氧化物酶(GPX)和还原型酶(GR)活性作为细胞氧化状态的标志。用0.5~10mU g/mLDCM处理培养的HepG2细胞2或20h，可完全阻止细胞损伤和GR的增加，并能部分阻止t-BOOH引起的GSH的降低和丙二醛和GPx的升高。相反，用DCM处理细胞时，t-BOOH诱导的ROS生成增加并未被阻止。结果表明，在预期的生理范围内用DCM浓度处理HepG2细胞可以显著保护细胞免受氧化损伤。
Soluble high-molecular weight fraction (named melanoidin) from coffee brew was isolated by ultrafiltration, subsequently digested by simulating a gastric plus pancreatic digestive condition and partly characterized by CZE, gel-filtration and browning. The objective of the present study was to investigate the potential protective effect of the coffee melanoidin submitted to gastrointestinal digestion on cell viability (lactate dehydrogenase leakage) and redox status of cultured human hepatoma HepG2 cells submitted to oxidative stress induced by tert-butylhydroperoxide (t-BOOH). Concentration of reduced glutathione (GSH) and malondialdehyde (MDA), generation of reactive oxygen species (ROS) and activity of antioxidant enzymes glutathione peroxidase (GPx) and reductase (GR) were used as markers of cellular oxidative status. Pretreatment of cultured HepG2 cells with 0.5-10 mu g/ mL digested coffee melanoidin (DCM) for 2 or 20 h completely prevented the increase in cell damage and GR and partly prevented the decrease of GSH and the increase of MDA and GPx evoked by t-BOOH in HepG2 cells. In contrast, increased ROS generation induced by t-BOOH was not prevented when cells were pretreated with DCM. The results show that treatment of HepG2 cells with concentrations of DCM within the expected physiological range confers the cells a significant protection against an oxidative insult.