Coconut oil meal, a cheap by-product of coconut oil production, is a rich source of phenolic antioxidants. Many age-related diseases are caused by reactive oxygen species- (ROS-) induced damage to macromolecules such as lipids, proteins, and DNA. In the present study, the protective effect of the phenolic extract of coconut oil meal (CMPE) against macromolecular oxidative damage was evaluated using in vitro and in vivo models. Sunflower oil, bovine serum albumin (BSA), and plasmid DNA were used in the in vitro study, and thiobarbituric acid reactive substances (TBARS), protein carbonyl, and nicked DNA were evaluated as oxidation products. The inhibitory effect of CMPE against H2O2-induced macromolecular damage was evaluated using cultured HEp-2 cells. The results indicate that CMPE inhibits macromolecular damage both in vitro and in vivo. In addition, CMPE regulates redox status of HEp-2 cells under oxidative stress conditions by maintaining higher reduced glutathione levels. There was no significant difference in the expression of glutathione peroxidase in stressed and unstressed cells suggesting that CMPE regulates the cellular oxidative stress responses without affecting the expression of oxidative stress response genes. Oral feeding of Wistar rats with CMPE improves the serum and plasma antioxidant status without causing any toxic effects.

中文翻译：

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椰子油膳食酚类抗氧化剂对大分子损伤的保护作用：体外和体内研究

椰子油粉是椰子油生产的一种廉价副产品，是酚类抗氧化剂的丰富来源。许多与年龄相关的疾病是由活性氧 (ROS) 对脂质、蛋白质和 DNA 等大分子引起的损伤引起的。在本研究中，使用体外和体内模型评估了椰子油粕酚提取物 (CMPE) 对大分子氧化损伤的保护作用。向日葵油、牛血清白蛋白 (BSA) 和质粒 DNA 用于体外研究，硫代巴比妥酸反应物质 (TBARS)、蛋白质羰基和带切口的 DNA 被评估为氧化产物。使用培养的 HEp-2 细胞评估 CMPE 对 H2O2 诱导的大分子损伤的抑制作用。结果表明，CMPE 在体外和体内均抑制大分子损伤。此外，CMPE 通过维持较高的还原型谷胱甘肽水平来调节氧化应激条件下 HEp-2 细胞的氧化还原状态。应激和非应激细胞中谷胱甘肽过氧化物酶的表达没有显着差异，表明 CMPE 调节细胞氧化应激反应而不影响氧化应激反应基因的表达。口服 CMPE 的 Wistar 大鼠可改善血清和血浆的抗氧化状态，而不会引起任何毒性作用。应激和非应激细胞中谷胱甘肽过氧化物酶的表达没有显着差异，表明 CMPE 调节细胞氧化应激反应而不影响氧化应激反应基因的表达。口服 CMPE 的 Wistar 大鼠可改善血清和血浆的抗氧化状态，而不会引起任何毒性作用。应激和非应激细胞中谷胱甘肽过氧化物酶的表达没有显着差异，表明 CMPE 调节细胞氧化应激反应而不影响氧化应激反应基因的表达。口服 CMPE 的 Wistar 大鼠可改善血清和血浆的抗氧化状态，而不会引起任何毒性作用。