Catechols in caffeic acid phenethyl ester are essential for inhibition of TNF‐mediated IP‐10 expression through NF‐κB‐dependent but HO‐1‐ and p38‐independent mechanisms in mouse intestinal epithelial cells

Mapesa, Job; Waldschmitt, Nadine; Schmoeller, Ingrid; Blume, Carolin; Hofmann, Thomas; Mahungu, Symon M.; Clavel, Thomas; Haller, Dirk

doi:10.1002/mnfr.201100105

Cited by 20 publications

(16 citation statements)

References 53 publications

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“…Therefore the finding that the anti-inflammatory properties of NOD rely on its redox activity was not surprising and compatible with published studies on polyphenols [55], [56]. Our data are also in line with a previously published study in which it was shown that catechols in caffeic acid phenethyl ester (CAPE) selectively inhibit NFκB target genes [17].…”

Section: Discussionsupporting

confidence: 92%

“…While it has been unambiguously demonstrated that a number of polyphenols possess strong anti-inflammatory action, the underlying mechanism has been equivocally discussed in recent years. Although tested in different cells or cell lines obtained from different species, Nrf-2 mediated induction of HO-1 [15], [16], inhibition of NFκB [16], [17] and inhibition of PLA2 [13] all seems to be pivotal or contributing to the anti-inflammatory action.…”

Section: Introductionmentioning

confidence: 99%

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N-Octanoyl Dopamine Inhibits the Expression of a Subset of κB Regulated Genes: Potential Role of p65 Ser276 Phosphorylation

et al. 2013

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Background and PurposeCatechol containing compounds have anti-inflammatory properties, yet for catecholamines these properties are modest. Since we have previously demonstrated that the synthetic dopamine derivative N-octanoyl dopamine (NOD) has superior anti-inflammatory properties compared to dopamine, we tested NOD in more detail and sought to elucidate the molecular entities and underlying mechanism by which NOD down-regulates inflammation.Experimental ApproachGenome wide gene expression profiling of human umbilical vein endothelial cells (HUVECs) was performed after stimulation with TNF-α or in the combination with NOD. Confirmation of these differences, NFκB activation and the molecular entities that were required for the anti-inflammatory properties were assessed in subsequent experiments.Key ResultsDown regulation of inflammatory genes by NOD occurred predominantly for κB regulated genes, however not all κB regulated genes were affected. These findings were explained by inhibition of RelA phosphorylation at Ser276. Leukocyte adherence to TNF-α stimulated HUVECs was inhibited by NOD and was reflected by a diminished expression of adhesion molecules on HUVECs. NOD induced HO-1 expression, but this was not required for inhibition of NFκB. The anti-inflammatory effect of NOD seems to involve the redox active catechol structure, although the redox active para-dihydroxy benzene containing compounds also displayed anti-inflammatory effects, provided that they were sufficiently hydrophobic.Conclusions and ImplicationsThe present study highlighted important mechanisms and molecular entities by which dihydroxy benzene compounds exert their potential anti-inflammatory action. Since NOD does not have hemodynamic properties, NOD seems to be a promising candidate drug for the treatment of inflammatory diseases.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

N-Octanoyl Dopamine Inhibits the Expression of a Subset of κB Regulated Genes: Potential Role of p65 Ser276 Phosphorylation

et al. 2013

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“…The second mechanism could be triggered by the ability of the phenolic and flavonoid compounds like quercetin, CAPE, p -vanillin, p -coumaric acid, apigenin, and cinnamic acid, all of which are present in Chilean propolis, to neutralize oxidative species [38]. CAPE not only has been shown to inhibit activation of the nuclear transcription factor- (NF-) κ B signaling pathway [39], but also has strong ROS scavenging ability and activates NrF2 [40], thereby increasing an antioxidant stress response, which could in part explain the antioxidant effects observed in our study related to the increase in GSH and decrease of TBARS.…”

Section: Discussionmentioning

confidence: 99%

The Role of Propolis in Oxidative Stress and Lipid Metabolism: A Randomized Controlled Trial

Mujica

Orrego

Pérez

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Although there is evidence of the benefits of propolis on human health, the vast majority of studies have been conducted using animal models. The present study includes the chemical characterization and clinical evaluation of the effects of the oral administration of propolis solution on the oxidative status and modulation of lipids in a human population in Talca, Chile. Chemical characterization of propolis, total phenol, flavonoids, and total antioxidant capacity were determined by ORAC. Identification of phenols and flavonoids in propolis was assessed by HPLC-DAD. A double-blind, placebo-controlled clinical trial was conducted. Subjects provided informed consent form and the Bioethics Committee of the Universidad de Talca approved protocol. Eligible subjects (n = 67) were randomized in two groups: propolis (n = 35) and placebo (n = 32). All subjects were evaluated at 0 (baseline), 45, and 90 days. In the propolis group, we observed that increases in HDL-c went from 53.9 ± 11.9 to 65.8 ± 16.7 mg/dL (p < 0.001) from baseline to 90 days. Compared to placebo subjects, consumption of propolis induced a net increase in GSH levels (p < 0.0001) and a decrease (p < 0.001) in TBARS levels for the propolis group. Our findings indicate potential benefits of propolis use in human health. The use of propolis appears to have positive effects on oxidative status and improvement of HDL-c, both of which contribute to a reduced risk of cardiovascular disease.

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“…CAPE has been reported to have biological and pharmacological activities including antioxidant [9,10,11,12,13,14], anti-inflammatory [15,16], antiviral [17], anti-carcinogenic [18], and immunomodulating effects [6]. CAPE has demonstrated a potent antioxidant activity in previous studies using an in vitro model [9,10,11,12] as well as an in vivo animal model [13,14].…”

Section: Introductionmentioning

confidence: 99%

Nrf2-Mediated HO-1 Induction Coupled with the ERK Signaling Pathway Contributes to Indirect Antioxidant Capacity of Caffeic Acid Phenethyl Ester in HepG2 Cells

Kim

Jang

2014

IJMS

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The objective of this study is to investigate the contributing effect of the nuclear transcription factor-erythroid 2-related factor 2 (Nrf2)-mediated signaling pathway on the indirect antioxidant capacity of caffeic acid phenethyl ester (CAPE) against oxidative stress in HepG2 cells. The result of an antioxidant response element (ARE)-luciferase assay showed that CAPE stimulated ARE promoter activity resulting in increased transcriptional and translational activities of heme oxygenase-1 (HO-1). In addition, CAPE treatment enhanced Nrf2 accumulation in the nucleus and the post-translational phosphorylation level of extracellular signal-regulated kinase (ERK) among several protein kinases tested. Treatment with ERK inhibitor U126 completely suppressed CAPE-induced ERK phosphorylation and HO-1 expression, but it only partly inhibited CAPE-induced Nrf2 accumulation and ARE promoter. Using the 2',7'-dichlorofluorescein-diacetate (DCFH-DA) method, the cellular antioxidant capacity of CAPE against 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH)- or H2O2-induced oxidative stress also was shown to be partially suppressed by the ERK inhibitor. From the overall results it is proposed that the indirect antioxidant activity of CAPE against oxidative stress in HepG2 cells is partially attributed to induction of HO-1, which is regulated by Kelch-like erythroid-cell-derived protein with CNC homology (ECH)-associated protein 1 (Keap1)-independent Nrf2 activation relying on post-translational phosphorylation of ERK.

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Catechols in caffeic acid phenethyl ester are essential for inhibition of TNF‐mediated IP‐10 expression through NF‐κB‐dependent but HO‐1‐ and p38‐independent mechanisms in mouse intestinal epithelial cells

Abstract: This study reveals the structure-activity effects and anti-inflammatory potential of CAPE in the intestinal epithelium.

Cited by 20 publications

References 53 publications

N-Octanoyl Dopamine Inhibits the Expression of a Subset of κB Regulated Genes: Potential Role of p65 Ser276 Phosphorylation

N-Octanoyl Dopamine Inhibits the Expression of a Subset of κB Regulated Genes: Potential Role of p65 Ser276 Phosphorylation

The Role of Propolis in Oxidative Stress and Lipid Metabolism: A Randomized Controlled Trial

Nrf2-Mediated HO-1 Induction Coupled with the ERK Signaling Pathway Contributes to Indirect Antioxidant Capacity of Caffeic Acid Phenethyl Ester in HepG2 Cells

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