Anti-Inflammatory Activity of Gallic Acid

Kroes, B. H.; Berg, A. J. J. van den; Ufford, H. C. Quarles van; Dijk, Hans van; Labadie, R. P.

doi:10.1055/s-2006-961535

Cited by 381 publications

(229 citation statements)

References 7 publications

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“…Similarly to another type of vinegar, coconut water vinegar also contains gallic and vanillic acids [18]. Gallic and vanillic acids have been reported to have antioxidant, anti-inflammatory [41,42], hypolipidaemic, and liver-protective effects on HFD-induced obese rat models [42,43]. Adipokines were also correlated with obesity-related inflammation.…”

Section: Discussionmentioning

confidence: 99%

Dietary coconut water vinegar for improvement of obesity-associated inflammation in high-fat-diet-treated mice

Mohamad

Yeap

Kỳ

et al. 2017

Food & Nutrition Research

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Obesity has become a serious health problem worldwide. Various types of healthy food, including vinegar, have been proposed to manage obesity. However, different types of vinegar may have different bioactivities. This study was performed to evaluate the anti-obesity and anti-inflammatory effects of coconut water vinegar on high-fat-diet (HFD)-induced obese mice. Changes in the gut microbiota of the mice were also evaluated. To induce obesity, C57/BL mice were continuously fed an HFD for 33 weeks. Coconut water vinegar (0.08 and 2 ml/kg body weight) was fed to the obese mice from early in week 24 to the end of week 33. Changes in the body weight, fat-pad weight, serum lipid profile, expression of adipogenesis-related genes and adipokines in the fat pad, expression of inflammatory-related genes, and nitric oxide levels in the livers of the untreated and coconut water vinegar-treated mice were evaluated. Faecal samples from the untreated and coconut water vinegar-treated mice (2 ml/kg body weight) were subjected to 16S metagenomic analysis to compare their gut microbiota. The oral intake of coconut water vinegar significantly (p < 0.05) reduced the body weight, fat-pad weight, and serum lipid profile of the HFD-induced obese mice in a dose-dependent manner. We also observed up-regulation of adiponectin and down-regulation of sterol regulatory element-binding protein-1, retinol-binding protein-4, and resistin expression. The coconut water vinegar also reduced HFD-induced inflammation by down-regulating nuclear factor-κB and inducible nitric oxide synthase expression, which consequently reduced the nitric oxide level in the liver. Alterations in the gut microbiota due to an increase in the populations of the Bacteroides and Akkermansia genera by the coconut water vinegar may have helped to overcome the obesity and inflammation caused by the HFD. These results provide valuable insights into coconut water vinegar as a potential food ingredient with anti-obesity and anti-inflammatory effects.

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Section: Discussionmentioning

confidence: 99%

Dietary coconut water vinegar for improvement of obesity-associated inflammation in high-fat-diet-treated mice

Mohamad

Yeap

Kỳ

et al. 2017

Food & Nutrition Research

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“…Although this effect with quercetin was observed in fMLP-stimulated rabbit PMNs (Takemura et al, 1997), it cannot be excluded that this also occurred under the conditions of our experiments with human blood. Gallic acid can inhibit degranulation of PMNs and interfere with the assembly of active NADPH-oxidase (Kroes et al, 1992). Accordingly, its inhibitory effect on fMLP-LBCL can also involve specific inhibition of signal transduction in human PMNs.…”

Section: Effect Of Polyphenols On Fmlp-induced Luminol Enhanced Wholementioning

confidence: 99%

Inhibitory effect of plant phenolics on fMLP-induced intracellular calcium rise and chemiluminescence of human polymorphonuclear leukocytes and their chemotactic activityin vitro

Nowak

Zasowska-Nowak

Białasiewicz

et al. 2015

Pharmaceutical Biology

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Context: Polymorphonuclear leukocytes (PMNs) produce oxidants, contributing to systemic oxidative stress. Diets rich in plant polyphenols seem to decrease the risk of oxidative stressinduced disorders including cardiovascular disease. Objective: The objective of this study was to examine the in vitro effect of each of the 14 polyphenols on PMNs chemotaxis, intracellular calcium response, oxidants production. Materials and methods: Blood samples and PMNs suspensions were obtained from 60 healthy non-smoking donors and incubated with a selected polyphenol (0.5-10 mM) or a control solvent. We assessed resting and fMLP-dependent changes of intracellular calcium concentration ([Ca 2+ ] i ) in PMNs with the Fura-2AM method and measured fMLP-induced luminol enhanced whole blood chemiluminescence (fMLP-LBCL). Polyphenol chemoattractant activity for PMNs was tested with Boyden chambers. Results: Polyphenols had no effect on resting [Ca 2+ ] i . Unaffected by other compounds, fMLPdependent increase of [Ca 2+ ] i was inhibited by quercetin and catechol (5 mM) by 32 ± 14 and 12 ± 10% (p50.04), respectively. Seven of the 14 tested substances (5 mM) influenced fMLP-LBCL by decreasing it. Catechol, quercetin, and gallic acid acted most potently reducing fMLP-LBCL by 49 ± 5, 42 ± 15, and 28 ± 18% (p50.05), respectively. 3,4-Dihydroxyhydrocinnamic, 3,4-dihydroxyphenylacetic, 4-hydroxybenzoic acid, and catechin (5 mM) revealed distinct (p50.02) chemoattractant activity with a chemotactic index of 1.9 ± 0.8, 1.8 ± 0.7, 1.6 ± 0.6, 1.4 ± 0.2, respectively. Conclusion and discussion: Catechol, quercetin, and gallic acid at concentrations commensurate in human plasma strongly suppressed the oxidative response of PMNs. Regarding quercetin and catechol, this could result from an inhibition of [Ca 2+ ] i response.

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“…Gallic acid is cytotoxic to cancer cells and has anti-inflammatory and antimutagenic properties (2,3). Gallic acid has been described as an excellent free radical scavenger and as an inducer of differentiation and programmed cell death in a number of tumor cell lines (4,5).…”

Section: Introductionmentioning

confidence: 99%

Gallic Acid Suppresses Lipopolysaccharide-Induced Nuclear Factor-κB Signaling by Preventing RelA Acetylation in A549 Lung Cancer Cells

Choi

Lee

Jung

et al. 2009

Molecular Cancer Research

145

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Although multiple studies have revealed that gallic acid plays an important role in the inhibition of malignant transformation, cancer development, and inflammation, the molecular mechanism of gallic acid in inflammatory diseases is still unclear. In this study, we identified gallic acid from Rosa rugosa as a histone acetyltransferase (HAT) inhibitor with global specificity for the majority of HAT enzymes, but with no activity toward epigenetic enzymes including sirtuin (silent mating type information regulation 2 homologue) 1 (S. cerevisiae), histone deacetylase, and histone methyltransferase. Enzyme kinetic studies indicated that gallic acid uncompetitively inhibits p300/CBP-dependent HAT activities. We found that gallic acid inhibits p300-induced p65 acetylation, both in vitro and in vivo, increases the level of cytosolic IκBα, prevents lipopolysaccharide (LPS)-induced p65 translocation to the nucleus, and suppresses LPS-induced nuclear factor-κB activation in A549 lung cancer cells. We have also shown that gallic acid treatment inhibits the acetylation of p65 and the LPS-induced serum levels of interleukin-6 in vivo. Importantly, gallic acid generally inhibited inflammatory responses caused by other stimuli, including LPS, IFN-γ, and interleukin-1β, and further downregulated the expression of nuclear factor-κB-regulated antiapoptotic genes. These results show the crucial role of acetylation in the development of inflammatory diseases. (Mol Cancer Res 2009;7(12):2011-21)

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Anti-Inflammatory Activity of Gallic Acid

Cited by 381 publications

References 7 publications

Dietary coconut water vinegar for improvement of obesity-associated inflammation in high-fat-diet-treated mice

Dietary coconut water vinegar for improvement of obesity-associated inflammation in high-fat-diet-treated mice

Inhibitory effect of plant phenolics on fMLP-induced intracellular calcium rise and chemiluminescence of human polymorphonuclear leukocytes and their chemotactic activityin vitro

Gallic Acid Suppresses Lipopolysaccharide-Induced Nuclear Factor-κB Signaling by Preventing RelA Acetylation in A549 Lung Cancer Cells

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