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首页> 外文期刊>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:通过抑制Caspase-3活化抑制氧化应激介导的内皮细胞损伤,蓝贻贝(Mytilus edulis)水解产物的氨基酸组成,抗氧化剂和细胞保护作用

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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 H 2 O 2 -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 Cu 2+ -mediated low density lipoprotein (LDL) oxidation. Treatment of H 2 O 2 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 H 2 O 2 -mediated oxidative stress in HUVECs. Flow cytometry and western blot analysis revealed that BMCH pre-treatment significantly reduced H 2 O 2 -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,我们研究了蓝贻贝(Mytilus edulis)水解产物对H 2 O 2介导的人脐静脉内皮细胞(HUVECs)氧化损伤的保护作用。蓝色贻贝水解产物是通过八种蛋白酶的酶促水解制备的,与其他水解产物相比,蓝色贻贝-α-胰凝乳蛋白酶水解产物(BMCH)在DPPH自由基清除,ABTS +自由基清除和ORAC值方面显示出最高的抗氧化活性。 BMCH还抑制Cu 2+介导的低密度脂蛋白(LDL)氧化。 H 2 O 2的处理导致HUVEC活力降低,而BMCH预处理则增加了HUVEC活力并减少了活性氧(ROS)的产生。 BMCH预处理提高了细胞抗氧化剂的能力,包括针对HUVEC中H 2 O 2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预处理通过抑制caspase-3激活而显着降低H 2 O 2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可以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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