186, Korea; [email protected] Division of Marine-Bio Convergence Science, Pukyong
186, Korea; [email protected] Division of Marine-Bio Convergence Science, Pukyong National University, Busan 48547, Korea Correspondence: [email protected] These authors contributed equally to this function.Citation: Suryaningtyas, I.T.; Ahn, C.-B.; Je, J.-Y. Cytoprotective Peptides from Blue Mussel Protein Hydrolysates: Identification and Mechanism Investigation in Human Umbilical Vein Endothelial Cells Injury. Mar. Drugs 2021, 19, 609. https://doi.org/10.3390/md19110609 Academic Editors: Donatella Degl’Innocenti and Marzia Vasarri Received: 9 October 2021 Accepted: 26 October 2021 Published: 27 OctoberAbstract: Cardiovascular disease represents a leading result in of mortality and is generally characterized by the emergence of endothelial dysfunction (ED), a physiologic condition that takes place within the early progress of atherosclerosis. Within this study, two cytoprotective peptides derived from blue mussel chymotrypsin hydrolysates together with the sequence of EPTF and FTVN had been purified and identified. Molecular mechanisms underlying the cytoprotective effects against oxidative tension which lead to human umbilical vein endothelial cells (HUVEC) injury had been investigated. The results showed that pretreatment of EPTF, FTVN and their mixture (1:1) in 0.1 mg/mL considerably reduced HUVEC death because of H2 O2 exposure. The cytoprotective mechanism of these peptides involves an improvement in the cellular antioxidant defense technique, as indicated by the suppression of your intracellular ROS generation through upregulation on the cytoprotective enzyme heme oxygenase-1. Also, H2 O2 exposure triggers HUVEC harm through the apoptosis procedure, as evidenced by elevated cytochrome C release, Bax protein expression, and the elevated level of activated caspase-3, having said that in HUVEC pretreated with peptides and their mixture, the presence of those apoptotic Cholesteryl sulfate MedChemExpress stimuli was significantly decreased. Each peptide showed equivalent cytoprotective effect but no synergistic effect. Taken with each other, these peptides could be especially essential in GSK2646264 LRRK2 safeguarding against oxidative stress-mediated ED. Search phrases: bioactive peptide; cytoprotective; oxidative tension; endothelial dysfunction; blue mussel1. Introduction The imbalance among the antioxidant defense mechanism and reactive oxygen species (ROS) generation within a physiological method results in oxidative tension and connected disease consequences. Regulated ROS generation is vital for the activation of protective signaling pathways, but when in excess amount it induces oxidative tension. Oxidative stress induces depolarization on the mitochondrial membrane. When the mitochondrial membrane potential is decreased, a series of signaling proteins is activated, which leads to the activation of many stress-responsive genes, for example p53, Bax, Bcl-2, and caspase-3 [1]. This leads to enhanced reactive oxygen species generation, extreme cell damage, and apoptosisinduced cell death [2,3]. These danger variables can induce endothelial dysfunction (ED) by means of a range of processes [4,5]. The endothelium, particularly the terminal arteries, is damaged by an excessive amount of ROS, which disrupts the intracellular reduction-oxidation balance. Therefore, ED is regarded as as an early indicator within the progression of cardiovascular illness (CVD) [6,7]. Considering the fact that oxidative pressure is defined as a achievable trigger of cardiovascular disease, treatment with antioxidants is actually a good technique to prevent CVD-causing endothelial vein harm. Recently, marine-derived food protein.
