Ferulic acid enhances the vasorelaxant effect of epigallocatechin gallate in tumor necrosis factor-alpha-induced inflammatory rat aorta

Jian Zhao, Aki Suyama, Mitsuru Tanaka, Toshiro Matsui

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Previously, we demonstrated synergistic enhancement of vasorelaxation by combination treatment with Trp-His and epigallocatechin gallate (EGCg) in intact rat aorta. The aim of the present study was to determine whether this vasorelaxant synergy could be recapitulated in tumor necrosis factor-alpha (TNF-α)-induced inflammatory rat aorta, and to determine the extent of its modulation by anti-inflammatory phenolic acids. Synergistic enhancement of vasorelaxation in rat aorta by Trp-His and EGCg was significantly attenuated in the presence of TNF-α, an effect that was reversed by the addition of ferulic acid (FA, 250 μM). Moreover, FA markedly enhanced EGCg-induced vasorelaxation, but not Trp-His-induced vasorelaxation, in TNF-α-treated aorta. Structure-activity analysis showed that the unsaturated 2-propenoic moiety and the methoxy group of FA were important for the enhancement of vasorelaxation by EGCg. The stimulation of EGCg-induced vasorelaxation by FA was antagonized by the nitric oxide synthase inhibitor NG-monomethyl-l-arginine acetate, while FA enhanced vasorelaxant properties of the endothelial nitric oxide (NO) synthase activator acetylcholine in TNF-α-treated inflammatory aorta. Moreover, the EGCg-stimulated NO production was also enhanced by FA in TNF-α-treated aorta. These data indicate that stimulation of NO production by FA enhances the vasorelaxant properties of EGCg in TNF-α-induced inflammatory aorta.

Original languageEnglish
Pages (from-to)807-814
Number of pages8
JournalJournal of Nutritional Biochemistry
Volume25
Issue number7
DOIs
Publication statusPublished - Jan 1 2014

Fingerprint

ferulic acid
Vasodilator Agents
tryptophyl-histidine
Aorta
Rats
Vasodilation
Tumor Necrosis Factor-alpha
Nitric Oxide
Nitric Oxide Synthase Type III
epigallocatechin gallate
Nitric Oxide Synthase
Acetylcholine
Arginine

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Molecular Biology
  • Nutrition and Dietetics
  • Clinical Biochemistry

Cite this

@article{72de85cf1bea45729d7ec1378d0c6a98,
title = "Ferulic acid enhances the vasorelaxant effect of epigallocatechin gallate in tumor necrosis factor-alpha-induced inflammatory rat aorta",
abstract = "Previously, we demonstrated synergistic enhancement of vasorelaxation by combination treatment with Trp-His and epigallocatechin gallate (EGCg) in intact rat aorta. The aim of the present study was to determine whether this vasorelaxant synergy could be recapitulated in tumor necrosis factor-alpha (TNF-α)-induced inflammatory rat aorta, and to determine the extent of its modulation by anti-inflammatory phenolic acids. Synergistic enhancement of vasorelaxation in rat aorta by Trp-His and EGCg was significantly attenuated in the presence of TNF-α, an effect that was reversed by the addition of ferulic acid (FA, 250 μM). Moreover, FA markedly enhanced EGCg-induced vasorelaxation, but not Trp-His-induced vasorelaxation, in TNF-α-treated aorta. Structure-activity analysis showed that the unsaturated 2-propenoic moiety and the methoxy group of FA were important for the enhancement of vasorelaxation by EGCg. The stimulation of EGCg-induced vasorelaxation by FA was antagonized by the nitric oxide synthase inhibitor NG-monomethyl-l-arginine acetate, while FA enhanced vasorelaxant properties of the endothelial nitric oxide (NO) synthase activator acetylcholine in TNF-α-treated inflammatory aorta. Moreover, the EGCg-stimulated NO production was also enhanced by FA in TNF-α-treated aorta. These data indicate that stimulation of NO production by FA enhances the vasorelaxant properties of EGCg in TNF-α-induced inflammatory aorta.",
author = "Jian Zhao and Aki Suyama and Mitsuru Tanaka and Toshiro Matsui",
year = "2014",
month = "1",
day = "1",
doi = "10.1016/j.jnutbio.2014.03.013",
language = "English",
volume = "25",
pages = "807--814",
journal = "Journal of Nutritional Biochemistry",
issn = "0955-2863",
publisher = "Elsevier Inc.",
number = "7",

}

TY - JOUR

T1 - Ferulic acid enhances the vasorelaxant effect of epigallocatechin gallate in tumor necrosis factor-alpha-induced inflammatory rat aorta

AU - Zhao, Jian

AU - Suyama, Aki

AU - Tanaka, Mitsuru

AU - Matsui, Toshiro

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Previously, we demonstrated synergistic enhancement of vasorelaxation by combination treatment with Trp-His and epigallocatechin gallate (EGCg) in intact rat aorta. The aim of the present study was to determine whether this vasorelaxant synergy could be recapitulated in tumor necrosis factor-alpha (TNF-α)-induced inflammatory rat aorta, and to determine the extent of its modulation by anti-inflammatory phenolic acids. Synergistic enhancement of vasorelaxation in rat aorta by Trp-His and EGCg was significantly attenuated in the presence of TNF-α, an effect that was reversed by the addition of ferulic acid (FA, 250 μM). Moreover, FA markedly enhanced EGCg-induced vasorelaxation, but not Trp-His-induced vasorelaxation, in TNF-α-treated aorta. Structure-activity analysis showed that the unsaturated 2-propenoic moiety and the methoxy group of FA were important for the enhancement of vasorelaxation by EGCg. The stimulation of EGCg-induced vasorelaxation by FA was antagonized by the nitric oxide synthase inhibitor NG-monomethyl-l-arginine acetate, while FA enhanced vasorelaxant properties of the endothelial nitric oxide (NO) synthase activator acetylcholine in TNF-α-treated inflammatory aorta. Moreover, the EGCg-stimulated NO production was also enhanced by FA in TNF-α-treated aorta. These data indicate that stimulation of NO production by FA enhances the vasorelaxant properties of EGCg in TNF-α-induced inflammatory aorta.

AB - Previously, we demonstrated synergistic enhancement of vasorelaxation by combination treatment with Trp-His and epigallocatechin gallate (EGCg) in intact rat aorta. The aim of the present study was to determine whether this vasorelaxant synergy could be recapitulated in tumor necrosis factor-alpha (TNF-α)-induced inflammatory rat aorta, and to determine the extent of its modulation by anti-inflammatory phenolic acids. Synergistic enhancement of vasorelaxation in rat aorta by Trp-His and EGCg was significantly attenuated in the presence of TNF-α, an effect that was reversed by the addition of ferulic acid (FA, 250 μM). Moreover, FA markedly enhanced EGCg-induced vasorelaxation, but not Trp-His-induced vasorelaxation, in TNF-α-treated aorta. Structure-activity analysis showed that the unsaturated 2-propenoic moiety and the methoxy group of FA were important for the enhancement of vasorelaxation by EGCg. The stimulation of EGCg-induced vasorelaxation by FA was antagonized by the nitric oxide synthase inhibitor NG-monomethyl-l-arginine acetate, while FA enhanced vasorelaxant properties of the endothelial nitric oxide (NO) synthase activator acetylcholine in TNF-α-treated inflammatory aorta. Moreover, the EGCg-stimulated NO production was also enhanced by FA in TNF-α-treated aorta. These data indicate that stimulation of NO production by FA enhances the vasorelaxant properties of EGCg in TNF-α-induced inflammatory aorta.

UR - http://www.scopus.com/inward/record.url?scp=84901841289&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84901841289&partnerID=8YFLogxK

U2 - 10.1016/j.jnutbio.2014.03.013

DO - 10.1016/j.jnutbio.2014.03.013

M3 - Article

C2 - 24794014

AN - SCOPUS:84901841289

VL - 25

SP - 807

EP - 814

JO - Journal of Nutritional Biochemistry

JF - Journal of Nutritional Biochemistry

SN - 0955-2863

IS - 7

ER -