Chicken Muscle Protein-Derived Peptide VVHPKESF Reduces TNFα-Induced Inflammation and Oxidative Stress by Suppressing TNFR1 Signaling in Human Vascular Endothelial Cells

Fan H, Bhullar KS, Wang Z, Wu J. Chicken Muscle Protein-Derived Peptide VVHPKESF Reduces TNFα-Induced Inflammation and Oxidative Stress by Suppressing TNFR1 Signaling in Human Vascular Endothelial Cells. Mol Nutr Food Res. 2022 Sep;66(17):e2200184. doi: 10.1002/mnfr.202200184. Epub 2022 Jul 20. PMID: 35770889.

PIP Author(s)

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About

Excessive and sustained inflammatory responses in the endothelial cells trigger vascular dysfunction, the key contributor to hypertension and atherosclerosis. Tumor necrosis factor alpha (TNFα), a pro-inflammatory cytokine, plays an important role in endothelial inflammatory responses cyclooxygenase 2 (COX2) and adhesion molecules including vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1). Over the years, food-derived bioactive peptides have been an emerging option for the prevention and treatment of hypertension and cardiovascular diseases. This study aims to investigate the protective effects of four chicken muscle-derived peptides Val-Arg-Pro (VRP), Leu-Lys-Tyr (LKY), Val-Arg-Tyr (VRY), and Val-Val-His-Pro-Lys-Glu-Ser-Phe [VVHPKESF (V-F)] on tumor necrosis factor alpha (TNFα)-induced endothelial inflammation and oxidative stress in human vascular endothelial
EA.hy926 cells.

Approach

EA.hy926 cells (passages 3–10) were grown in the growth medium in an incubator (37 °C) at 5% CO2 and 100% humidity. Chicken muscle-derived peptides were added into the cultured media to treat the cells at the concentration of 25–100 μM for different periods of time (within 24 h). Cells were grown on 24-well plates until reaching confluence, followed by peptide treatment for 18 h before another 6 h of TNFα stimulation (10 ng mL−1). Cells without peptide or TNFα treatment were used as the control group.

Analysis of Results

Inflammation and oxidative stress are induced in EA.hy926 cells by TNFα (10 ng mL−1) treatment for different periods of time. Inflammatory proteins and signaling molecules including inducible nitric oxide synthase, intracellular cell adhesion molecule-1, vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase 2 (COX2), nuclear factor kappa B (NF-kB), mitogen-activated protein kinases (MAPKs), and TNFα receptor 1 (TNFR1) are measured by qRT-PCR or western blotting; soluble TNFR1 level and nicotinamide adenine dinucleotide phosphate NADPH) oxidase activity are determined by Elisa kits; superoxide is measured by dihydroethidium staining. Only V-F treatment inhibits the expression of VCAM-1 and COX2, via suppressing NF-kB and p38 MAPK signaling, respectively, while reduced oxidative stress via the inhibition of NADPH oxidase activity; V-F treatment attenuates both gene and protein expressions of TNFR1.

Application

V-F treatment ameliorates TNFα-induced endothelial inflammation and oxidative stress likely via the inhibition of TNFR1 signaling, suggesting its potential as a functional food ingredient or nutraceutical in the prevention and treatment of hypertension and cardiovascular diseases.

Abstract

This study aims to investigate the protective effects of four chicken muscle-derived peptides Val-Arg-Pro (VRP), Leu-Lys-Tyr (LKY), Val-Arg-Tyr (VRY), and Val-Val-His-Pro-Lys-Glu-Ser-Phe [VVHPKESF (V-F)] on tumor necrosis factor alpha (TNFα)-induced endothelial inflammation and oxidative stress in human vascular endothelial EA.hy926 cells. Inflammation and oxidative stress are induced in EA.hy926 cells by TNFα (10 ng mL−1) treatment for different periods of time. Inflammatory proteins and signaling molecules including inducible nitric oxide synthase, intracellular cell adhesion molecule-1, vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase 2 (COX2), nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPKs), and TNFα receptor 1 (TNFR1) are measured by qRT-PCR or western blotting; soluble TNFR1 level and nicotinamide adenine dinucleotide phosphate NADPH) oxidase activity are determined by Elisa kits; superoxide is measured by dihydroethidium staining. Only V-F treatment inhibits the expression of VCAM-1 and COX2, via suppressing NF-κB and p38 MAPK signaling, respectively, while reduced oxidative stress via the inhibition of NADPH oxidase activity; V-F treatment attenuates both gene and protein expressions of TNFR1. V-F treatment ameliorates TNFα-induced endothelial inflammation and oxidative stress likely via the inhibition of TNFR1 signaling, suggesting its potential as a functional food ingredient or nutraceutical in the prevention and treatment of hypertension and cardiovascular diseases.