Format

Send to

Choose Destination
Mar Drugs. 2019 Feb 25;17(2). pii: E135. doi: 10.3390/md17020135.

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.

Author information

1
Department of Marine-Bio Convergence Science, Pukyong National University, Busan 48547, Korea. si565@daum.net.
2
Division of Food and Nutrition, Chonnam National University, Gwangju 61186, Korea. a321@jnu.ac.kr.
3
Food Safety and Processing Research Division, National Fisheries Research & Development Institute, Busan 4608, Korea. dennis011@korea.kr.
4
Food Safety and Processing Research Division, National Fisheries Research & Development Institute, Busan 4608, Korea. yeonkyekim@korea.kr.
5
Food Safety and Processing Research Division, National Fisheries Research & Development Institute, Busan 4608, Korea. dbssud@korea.kr.
6
Department of Marine-Bio Convergence Science, Pukyong National University, Busan 48547, Korea. jjy1915@pknu.ac.kr.

Abstract

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.

KEYWORDS:

bioactive peptide; blue mussel; caspase-3 activation; endothelial dysfunction; oxidative stress

PMID:
30823522
PMCID:
PMC6409750
DOI:
10.3390/md17020135
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
Loading ...
Support Center