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Dietary polyphenol canolol from rapeseed oil attenuates oxidative stress-induced cell damage through the modulation of the p38 signaling pathway

机译:菜籽油中的膳食多酚芥花酚通过调节p38信号通路来减轻氧化应激诱导的细胞损伤

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Canolol (CAO) is a main phenolic compound with remarkable antioxidative properties that is generated in rapeseed oil during microwave pressing. The objective of this study was to identify the protective effect of CAO in hydrogen peroxide (H _(2) O _(2) )-triggered oxidative stress and reveal the role of the p38 MAPK pathway during the protective process. CAO treatment showed an observable cytoprotective effect. Results showed that CAO significantly improved H _(2) O _(2) -stimulated cell death, and diminished ROS production and malondialdehyde (MDA) level. Moreover, CAO increased glutathione (GSH) content and promoted the activities of superoxide dismutase (SOD) and catalase (CAT). As a result, apoptosis was ameliorated and depletion of the mitochondrial membrane potential was restored. Western blotting analysis demonstrated CAO downregulated the expression of caspase-3 and decreased the ratio of Bax/Bcl-2. Notably, the phosphorylation of p38 MAPK was inhibited by CAO in H _(2) O _(2) -induced apoptosis, which was confirmed by its inhibitor (SB203580). Taken together, our study demonstrated the pivotal role of the p38 MAPK pathway in the cytoprotective effect of CAO on oxidative stress-induced cell damage, suggesting CAO is a promising antioxidant in food and health-related fields.
机译:卡诺洛尔(CAO)是一种具有显着抗氧化特性的主要酚类化合物,在微波压制过程中在菜籽油中产生。这项研究的目的是确定CAO在过氧化氢(H _(2)O _(2))触发的氧化应激中的保护作用,并揭示p38 MAPK途径在保护过程中的作用。 CAO处理显示出可观察到的细胞保护作用。结果表明,CAO显着改善了H _(2)O _(2)刺激的细胞死亡,并减少了ROS的产生和丙二醛(MDA)的水平。此外,CAO增加了谷胱甘肽(GSH)含量并促进了超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性。结果,细胞凋亡得到改善并且线粒体膜电位的消耗得以恢复。蛋白质印迹分析表明,CAO下调了caspase-3的表达,并降低了Bax / Bcl-2的比例。值得注意的是,p38 MAPK的磷酸化在H_(2)O_(2)诱导的细胞凋亡中被CAO抑制,这由其抑制剂(SB203580)证实。综上所述,我们的研究证明了p38 MAPK途径在CAO对氧化应激诱导的细胞损伤的细胞保护作用中的关键作用,表明CAO在食品和健康相关领域是一种有希望的抗氧化剂。

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