ReferenceID 6530
The anti-inflammatory effect of ε-viniferin by specifically targeting formyl peptide receptor 1 on human neutrophils
Chem Biol Interact
The uncontrol respiratory burst in neutrophils can lead to inflammation and tissue damage. This study investigates the effect and the underlying mechanism of epsilon-viniferin, a lignan from the root of Vitis thunbergii
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Record Fields
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- Reference Id
- 6530
- Evidence Id
- 23120
- Core Evidence Id
- 23120
- Source Reference Id
- 6361
- Herb2 Reference Id
- HBREF007158
- Subject Paper Key
- HBIN049233_34144024
- Pubmed Id
- 34144024
- Doi
- 10.1016/j.cbi.2021.109490
- Paper Title
- The anti-inflammatory effect of ε-viniferin by specifically targeting formyl peptide receptor 1 on human neutrophils
- Paper Abstract
- The uncontrol respiratory burst in neutrophils can lead to inflammation and tissue damage. This study investigates the effect and the underlying mechanism of epsilon-viniferin, a lignan from the root of Vitis thunbergii var. thunbergii, inhibits N-formyl-L-methionyl-L-leucyl-l-phenylalanine (fMLP) induced respiratory burst by antagonizing formyl peptide receptor 1 in human neutrophils. Briefly, epsilon-viniferin specifically inhibited fMLP (0.1 muM: formyl peptide receptor 1 agonist or 1 muM: formyl peptide receptor 1, 2 agonist)-induced superoxide anion production in a concentration-dependent manner (IC50 = 2.30 +- 0.96 or 9.80 +- 0.21 muM, respectively) without affecting this induced by formyl peptide receptor 2 agonist (WKYMVM). epsilon-viniferin inhibited fMLP (0.1 muM)-induced phosphorylation of ERK, Akt, Src or intracellular calcium mobilization without affecting these caused by WKYMVM. The synergistic suppression of fMLP (1 muM)-induced superoxide anion production was observed only in the combination of epsilon-viniferin and formyl peptide receptor 2 antagonist (WRW4) but not in combination of epsilon-viniferin and formyl peptide receptor 1 antagonist (cyclosporine H). epsilon-viniferin inhibited FITC-fMLP binding to formyl peptide receptors. Moreover, the synergistic suppression of FITC-fMLP binding was observation only in the combination of epsilon-viniferin and WRW4 but not in other combinations. ATPgammaS induced superoxide anion production through formyl peptide receptor 1 in fMLP desensitized neutrophils and this effect was inhibited by epsilon-viniferin. The concentration-response curve of fMLP-induced superoxide anion was not parallel shifted by epsilon-viniferin. Furthermore, the inhibiting effect of epsilon-viniferin on fMLP-induced superoxide anion production was reversible. These results suggest that epsilon-viniferin is an antagonist of formyl peptide receptor 1 in a reversible and non-competitive manner.
- Journal
- Chem Biol Interact
- Publish Year
- 2021
- Experiment Subject
- human; thunbergii
- Experiment Type
- Cell Experiment
- Phenotype Related
- Inflammation
- Paper Title Cn
- Paper Title En
- The anti-inflammatory effect of ε-viniferin by specifically targeting formyl peptide receptor 1 on human neutrophils
- Bilingual Status
- semi_complete