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.

Abstract

Scope: 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.

Methods and 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-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.

Conclusion: 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.

Keywords: NADPH; TNFR1; bioactive peptides; cellular mechanism; endothelial cell; inflammation; meat; oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chickens / metabolism
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Endothelial Cells
  • Humans
  • Inflammation / metabolism
  • Muscle Proteins / metabolism
  • NF-kappa B* / metabolism
  • Oxidative Stress
  • Receptors, Tumor Necrosis Factor, Type I / metabolism
  • Tumor Necrosis Factor-alpha* / metabolism
  • Tumor Necrosis Factor-alpha* / pharmacology
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Muscle Proteins
  • NF-kappa B
  • Receptors, Tumor Necrosis Factor, Type I
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Cyclooxygenase 2