首页> 美国卫生研究院文献>Marine Drugs >Amino Acid Composition Antioxidant and Cytoprotective Effect of Blue Mussel (Mytilus edulis) Hydrolysate through the Inhibition of Caspase-3 Activation in Oxidative Stress-Mediated Endothelial Cell Injury
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Amino Acid Composition Antioxidant and Cytoprotective Effect of Blue Mussel (Mytilus edulis) Hydrolysate through the Inhibition of Caspase-3 Activation in Oxidative Stress-Mediated Endothelial Cell Injury

机译:蓝贻贝(Mytilus edulis)水解产物通过抑制Caspase-3活化在氧化应激介导的内皮细胞损伤中的氨基酸组成抗氧化剂和细胞保护作用

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摘要

Enhanced oxidative stress plays a central role in promoting endothelial dysfunction, leading to the development of atherosclerosis. In this study, we investigated the protective effects of the hydrolysates derived from blue mussel (Mytilus edulis) against H2O2-mediated oxidative injury in human umbilical vein endothelial cells (HUVECs). The blue mussel hydrolysates were prepared by enzymatic hydrolysis with eight proteases, and blue mussel-α-chymotrypsin hydrolysate (BMCH) showed the highest antioxidant activities in DPPH radical scavenging, ABTS+ radical scavenging, and ORAC value compared to those of the other hydrolysates. BMCH also inhibited Cu2+-mediated low density lipoprotein (LDL) oxidation. Treatment of H2O2 resulted in the decreased HUVEC viability whereas pre-treatment with BMCH increased HUVEC viability and reduced reactive oxygen species (ROS) generation. BMCH pre-treatment increased cellular antioxidant capacities, including levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) against H2O2-mediated oxidative stress in HUVECs. Flow cytometry and western blot analysis revealed that BMCH pre-treatment significantly reduced H2O2-mediated HUVEC apoptosis through inhibition of caspase-3 activation. Real-time-qPCR analysis showed that BMCH down-regulated expression of p53 and caspase-3 genes, as well as decreased the bax/bcl-2 ratio. Taken together, these results indicate that BMCH may be useful as functional food ingredients for protecting endothelial dysfunction or related disease.
机译:增强的氧化应激在促进内皮功能障碍,导致动脉粥样硬化发展中起着核心作用。在这项研究中,我们调查了源自蓝贻贝(Mytilus edulis)的水解产物对H2O2介导的人脐静脉内皮细胞(HUVECs)氧化损伤的保护作用。蓝贻贝水解产物是通过8种蛋白酶的酶促水解制备的,蓝贻贝-α-胰凝乳蛋白酶水解产物(BMCH)在DPPH自由基清除,ABTS + 自由基清除中具有最高的抗氧化活性,并且ORAC值相比与其他水解产物相比。 BMCH还抑制Cu 2 + 介导的低密度脂蛋白(LDL)氧化。过氧化氢处理导致HUVEC活力降低,而BMCH预处理则提高了HUVEC活力并减少了活性氧(ROS)的产生。 BMCH预处理增加了细胞抗氧化剂的能力,包括针对HUVEC中H2O2介导的氧化应激的谷胱甘肽(GSH),超氧化物歧化酶(SOD),过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)的水平。流式细胞仪和蛋白质印迹分析表明,BMCH预处理可通过抑制caspase-3激活来显着减少H2O2介导的HUVEC凋亡。实时qPCR分析表明,BMCH下调了p53和caspase-3基因的表达,并降低了bax / bcl-2比率。综上所述,这些结果表明BMCH可用作保护内皮功能障碍或相关疾病的功能性食品成分。

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