Transcriptional regulation of cytokines and oxidative stress by gallic acid in human THP-1 monocytes

Gokulakrishnan, Kuppan; Balasubramanyam, Jayashree; Monickaraj, Finny; Srinivasan, Gayatri; Mohan, Viswanathan; Balasubramanyam, Muthuswamy

doi:10.1016/j.cyto.2009.11.003

Cited by 57 publications

(32 citation statements)

References 43 publications

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“…Another study reported that GA could attenuate the pro-inflammatory and pro-oxidant effects caused by tumor necrosis factor-α, interleukin-6, NADPH oxidase, and thioredoxin-interacting protein. It can also attenuate DNA damage and suppress hyperglycemia-induced activation of pro-inflammatory and pro-oxidant gene expression (17). The study by Kim et al (18) showed that GA was a histone acetyltransferase inhibitor and could suppress β-amyloid neurotoxicity by inhibiting microglial-mediated neuroinflammation.…”

Section: Introductionmentioning

confidence: 99%

Effect of JJYMD-C, a novel synthetic derivative of gallic acid, on proliferation and phenotype maintenance in rabbit articular chondrocytes in vitro

Lin

et al. 2014

Braz J Med Biol Res

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Tissue engineering encapsulated cells such as chondrocytes in the carrier matrix have been widely used to repair cartilage defects. However, chondrocyte phenotype is easily lost when chondrocytes are expanded in vitro by a process defined as “dedifferentiation”. To ensure successful therapy, an effective pro-chondrogenic agent is necessary to overcome the obstacle of limited cell numbers in the restoration process, and dedifferentiation is a prerequisite. Gallic acid (GA) has been used in the treatment of arthritis, but its biocompatibility is inferior to that of other compounds. In this study, we modified GA by incorporating sulfamonomethoxine sodium and synthesized a sulfonamido-based gallate, JJYMD-C, and evaluated its effect on chondrocyte metabolism. Our results showed that JJYMD-C could effectively increase the levels of the collagen II, Sox9, and aggrecan genes, promote chondrocyte growth, and enhance secretion and synthesis of cartilage extracellular matrix. On the other hand, expression of the collagen I gene was effectively down-regulated, demonstrating inhibition of chondrocyte dedifferentiation by JJYMD-C. Hypertrophy, as a characteristic of chondrocyte ossification, was undetectable in the JJYMD-C groups. We used JJYMD-C at doses of 0.125, 0.25, and 0.5 µg/mL, and the strongest response was observed with 0.25 µg/mL. This study provides a basis for further studies on a novel agent in the treatment of articular cartilage defects.

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Section: Introductionmentioning

confidence: 99%

Effect of JJYMD-C, a novel synthetic derivative of gallic acid, on proliferation and phenotype maintenance in rabbit articular chondrocytes in vitro

Lin

et al. 2014

Braz J Med Biol Res

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“…17 Prior studies have mainly demonstrated anticancer effects of GA relative to oxidative stress, Bcl-2, and the caspase family. [19][20][21][22] So the main purpose of our study was to investigate effects of GA on PCNA, which acts as a processivity factor for DNA polymerase d in eukaryotic cells, p53, which regulates cell cycle and functions as a tumor suppressor, and NF-kB, which is a transcription factor involved in cellular response to stimuli such as various stresses, cytokines, free radicals, etc.…”

Section: Discussionmentioning

confidence: 99%

Gallic Acid Inhibits Cell Viability and Induces Apoptosis in Human Monocytic Cell Line U937

Namseok

Jeong

Hwang

et al. 2011

Journal of Medicinal Food

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In the present study, we investigated the effects of gallic acid (GA) (3,4,5-trihydroxybenzoic acid), a polyhydroxyphenolic compound, isolated from Rhus chinensis, on the human monocytic lymphoma cell line U937. In vitro experiments showed that treating U937 cells with various amounts of GA inhibited cell viability and induced apoptosis in a dose-dependent manner. In order to understand the mechanism by which GA induces apoptosis, we examined the gene expression of p53, nuclear factor κB (NF-κB), and inhibitor of NF-κB (I-κB) after treating the cells with GA and found that expression levels of the genes for p53 and NF-κB increased and that for I-κB decreased. The results obtained from western blotting with U937 cells showed up-regulation of NF-κB protein and down-regulation of proliferating cell nuclear antigen and I-κB protein. These results demonstrate that GA efficiently induces apoptosis in U937 cells and that GA is a potential chemotherapeutic agent against lymphoma.

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“…Estas células han sido utilizadas en la prueba cometa para determinar la genotoxicidad de agentes contaminantes, micotoxinas y del trióxido de arsénico (otro inductor de ROS) entre otros (40)(41)(42). Igualmente se han utilizado en determinar el efecto protectivo del ácido gálico y de la fagocitosis de partículas de cromo y cobalto al efecto genotóxico (43,44). Algunos de estos ensayos además de analizar el daño directo al ADN (o SSB roturas en una sola cadena del ADN) han determinado el daño oxidativo de ADN utilizando enzimas como la formamido-pirimidinoglicosilasa (FPG) o la endonucleasa III que reconocen purinas o pirimidinas oxidadas, aumentando la especifi cidad y sensibilidad del ensayo al aumentar la migración del ADN.…”

Section: Discussionunclassified

Genotoxicidad del nifurtimox en deferentes líneas celulares utilizando el ensayo cometa

Escobar

2016

Rev. Médica Risaralda

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ResumenEl nifurtimox es un 5-nitrofurano sintético utilizado en el tratamiento de la enfermedad de Chagas. El objetivo de este estudio fue determinar la toxicidad celular y el daño del ADN causado por el nifurtimox en células Vero, J774, NIH/3T3 y THP-1. Se utilizó la coloración vital con azul tripan y el método colorimétrico MTT para determinar la toxicidad y el ensayo cometa alcalino para determinar el daño al ADN. Los cometas fueron contados en un microscopio de fluorescencia y el porcentaje de daño total del ADN fue calculado y clasificado de 0 (sin daño) a 4 (daño severo). En el ensayo de toxicidad, las células J774 fueron las líneas celulares más sensibles y las células THP-1 las menos sensibles al nifurtimox con valores de CC 50 34,04-138,58 µg/ml y CC 90 130,58->300 µg/ml de nifurtimox, respectivamente. En el ensayo cometa, el porcentaje de daño total de ADN a 100 µg/ml de nifurtimox fue 79,75%, 85,30% y 10,25% en células NIH/3T3, J774 y THP-1 respectivamente. En las células Vero el daño del ADN fue del 80% en células tratadas y no tratadas. El nifurtimox presentó toxicidad y genotoxicidad con actividades que dependieron del tipo de célula y de la concentración del medicamento utilizada. Es importante tomar en cuenta estas diferencias al realizar conclusiones finales de resultados obtenidos utilizando estos ensayos, especialmente el ensayo cometa.Palabras clave: nifurtimox; citotoxicidad; genotoxicidad; ensayo cometa; líneas celulares. Genotoxiciyt from Nifurtimox in comet assay AbstractNifurtimox is a synthetic 5-nitrofuran used in treating Chagas disease and potentially genotoxic in experimental models. The aim of this study was to determine the cell toxicities and DNA damage caused by nifurtimox on Vero, J774, NIH/3T3 and THP-1 cells. Vital trypan blue staining and MTT colorimetric test for cell toxicities and alkaline comet assay for DNA damage were performed. Comets were counted under fluorescent microscope and the % of DNA damage was calculated and scored from 0 (no damage) to 4 (high damage). J774 cells was the more sensitive and THP-1 cells the less one with values of CC 50 34.04-138.58µg/ml and CC 90 130.58->300 µg/ml. At a dose of 100 µg/ml of nifurtimox, DNA damage was 79.75, 85.30 % and 10.25% on NIH/3T3, J774 and THP-1 cells respectively. Vero cell showed 80% DNA damage in both treated and untreated cells. Both, cell toxicity and DNA damage were dependent on cell type and drug concentration. It is important to take these variables into account for final conclusions when these types of assays, especially comet assay are performed.Key words: nifurtimox; cytotoxicity; genotoxicity; comet assay; cell lines. IntroducciónEl nifurtimox (3-metil-4-(nitrofurfurilidenamina)-tetrahidro-4H-1,4-tiazina-1,1-dioxido, Lampit®, Bayer) es un 5-nitrofurano sintético utilizando en el tratamiento de enfermedades producidas por tripanosomas como la enfermedad de Chagas (Tripanosomiasis americana). La enfermedad de Chagas es una enfermedad sistémica compleja que afecta más de 7 millones de personas resultando en a...

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Transcriptional regulation of cytokines and oxidative stress by gallic acid in human THP-1 monocytes

Cited by 57 publications

References 43 publications

Effect of JJYMD-C, a novel synthetic derivative of gallic acid, on proliferation and phenotype maintenance in rabbit articular chondrocytes in vitro

Effect of JJYMD-C, a novel synthetic derivative of gallic acid, on proliferation and phenotype maintenance in rabbit articular chondrocytes in vitro

Gallic Acid Inhibits Cell Viability and Induces Apoptosis in Human Monocytic Cell Line U937

Genotoxicidad del nifurtimox en deferentes líneas celulares utilizando el ensayo cometa

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