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Clarion GO screen assay to assess gene expression responses of human SK-N-SH neuroblastoma cells under control and IL-1B induced conditions in response to herbal extracts of Sage (S. offinicalis) and Chamomile (C. nobile).

ABSTRACT: Chronic inflammation plays a critical role in the initiation and development of various human illnesses. The use of steroidal anti-inflammatory drugs (SAIDs) or non-steroidal anti-inflammatory drugs (NSAIDs) is now much more frequent and presents a number of unwanted side effects. For example long- or short-term usage of SAIDs presents multiple negative side effects such as stomach irritation, thinning of the skin, immune defence regression, weight gain and even sometimes a cortico-dependence, and NSAIDs have been linked to a higher risk of strokes, heart attacks, and heart-related deaths. In parallel, there has been renewed interest in alternative medicines and natural therapies and thousands of potential medicinal plants, including sage and chamomile. This study assesses the gene expression responses of human SK-N-SH neuroblastoma cells, pre-treated with aqueous ethanol extracts of sage (Salvia officinalis) or Roman chamomile (Chamaemelum nobile), following 4h or 24h treatment with IL-1B versus control conditions.

ORGANISM(S): Homo sapiens

SUBMITTER: Kieron Edwards

PROVIDER: E-MTAB-9611 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Clarion GO screen assay to assess gene expression responses of human mature adipocytes under control and IL-1B induced conditions in response to herbal extracts of Sage (S. offinicalis) and Chamomile (C. nobile).

Project description:Chronic inflammation plays a critical role in the initiation and development of various human illnesses. The use of steroidal anti-inflammatory drugs (SAIDs) or non-steroidal anti-inflammatory drugs (NSAIDs) is now much more frequent and presents a number of unwanted side effects. For example long- or short-term usage of SAIDs presents multiple negative side effects such as stomach irritation, thinning of the skin, immune defence regression, weight gain and even sometimes a cortico-dependence, and NSAIDs have been linked to a higher risk of strokes, heart attacks, and heart-related deaths. In parallel, there has been renewed interest in alternative medicines and natural therapies and thousands of potential medicinal plants, including sage and chamomile. This study assesses the gene expression responses of human mature adipopcytes (differentiated from fibroblastic pre-adipocytes [PromoCell, Germany; Catalogue #C-12730]), pre-treated with aqueous ethanol extract of sage (Salvia officinalis) or Roman chamomile (Chamaemelum nobile), following 4h or 24h treatment with IL-1B versus control conditions.

2020-10-05 | E-MTAB-9609 | biostudies-arrayexpress

Small molecule interactome mapping by photo-affinity labeling (SIM-PAL)

Project description:Non-steroidal anti-inflammatory drugs (NSAIDs) are one of the most common pharmaceutical agents in the world. However, despite well-studied interactions with cyclooxygenase-2, little is known about the broader proteomic interactions and additional mechanisms that the NSAIDs elicit. Here we present a global binding site identification platform for the direct in cellulo characterization of NSAID binding sites. The platform uses (1) photochemical conjugation of NSAID derivatives in the whole proteome, (2) enrichment of the binding sides, for (3) targeted mass spectrometry-based assignment. Using our approach, we identified the NSAID “interactome” consisting of nearly 200 binding sites in Jurkat and K562 cells. We observed a binding site hotspot on the nucleosome where three NSAIDs (but not fragment-based small molecules) interacted. These data suggest that the NSAIDs may behave as a novel type of epigenetic mark. Our approach is potentially amenable to production of precise, whole proteome binding site maps for virtually any molecule of interest.

2019-01-25 | PXD007094 | Pride

Mechanisms of pparγ activation by non-steroidal anti-inflammatory drugs and GQ16.

Project description:This study was undertaken to assess the similarities (or differences) between the well-established PPARγ agonist Rosiglitazone and Non-steroidal anti-inflammatory drugs (NSAIDs) diclofenac, indomethacin and ibuprofen, as well as the partial agonist GQ16 at the transcriptome level. Assessment of NSAID and GQ16 activities in PPARγ-dependent 3T3-L1 cells reveals that NSAIDs and GQ16 display similar effects toward PPARγ-dependent target genes in a manner similar to that of Rosiglitazone.

2015-06-01 | GSE64075 | GEO

Gene expression studies in IEC-6 cells induced by non-steroidal anti-inflammatory agents

Project description:Non-steroidal anti-inflammatory drugs (NSAIDs) are used extensively as therapeutic agents, despite their well-documented gastrointestinal (GI) toxicity. Presently, the mechanisms responsible for NSAID-associated GI damage are incompletely understood. In this study, we used Microarray analysis to generate a novel hypothesis about cellular mechanisms that underlie the GI toxicity of NSAIDs. Monolayers of intestinal epithelial cells (IEC-6) were treated with NSAIDs that either exhibit indomethacin, NS-398) or lack (SC-560) inhibitory effects on intestinal epithelial cell migration. Bioinformatic analysis of array data suggested that NSAIDs with adverse GI effects either decrease the gene expression of the calpains or increase the gene expression of the calpain engodenous inhibitor, calpastatin. Calpains have been shown previously to modulate the migration of a variety of cells in different physiological contexts. Our experimental results suggest that the altered expression of calpain genes may contribute to the adverse effects of NSAIDs on intestinal epithelial restitution. Microarray analysis has generated the novel hypothesis that the GI toxicity of NSAIDs may be attributed in part to drug-induced changes in the expression and activity of calpains. Keywords: dose response

2009-03-21 | GSE7584 | GEO

Transcription profiling of rat intestinal epithelial IEC-6 cells treated with non-steroidal anti-inflammatory agents to investigate gastrointestinal toxicity of NSAIDs

Project description:Non-steroidal anti-inflammatory drugs (NSAIDs) are used extensively as therapeutic agents, despite their well-documented gastrointestinal (GI) toxicity. Presently, the mechanisms responsible for NSAID-associated GI damage are incompletely understood. In this study, we used Microarray analysis to generate a novel hypothesis about cellular mechanisms that underlie the GI toxicity of NSAIDs. Monolayers of intestinal epithelial; cells (IEC-6) were treated with NSAIDs that either exhibit indomethacin, NS-398) or lack (SC-560) inhibitory effects on intestinal epithelial cell migration. Bioinformatic analysis of array data suggested that NSAIDs with adverse GI effects either decrease the gene expression of the calpains or increase the gene expression of the calpain engodenous; inhibitor, calpastatin. Calpains have been shown previously to modulate the migration of a variety of cells in different physiological contexts. Our experimental results suggest that the altered expression of calpain genes may contribute to the adverse effects of NSAIDs on intestinal; epithelial restitution. Microarray analysis has generated the novel hypothesis that the GI toxicity of NSAIDs may be attributed in part to drug-induced changes in the expression and activity of calpains. Experiment Overall Design: Monolayers of intestinal epithelial cells (IEC-6) were treated with NSAIDs that either exhibit (indomethacin, NS-398) or lack (SC-560) inhibitory effects on intestinal epithelial cell migration. Samples were then pooled to obtain sufficient material for gene array analysis. The pooled samples were used to hybridize 4 gene array chips for each biological sample.

2009-03-27 | E-GEOD-7584 | biostudies-arrayexpress

Non-steroidal Anti-inflammatory Drugs Decrease E2F1 Expression and Inhibit Cell Growth in Ovarian Cancer Cells

Project description:Epidemiological studies have shown that the regular use of non-steroidal anti-inflammatory (NSAIDs) drugs is associated with a reduced risk of various cancers. In addition, in vitro and experiments in mouse models have demonstrated that NSAIDs decrease tumor initiation and/or progression of several cancers. However, there are limited preclinical studies investigating the effects of NSAIDs in ovarian cancer. Here, we have studied the effects of two NSAIDs, diclofenac and indomethacin, in ovarian cancer cell lines and in a xenograft mouse model. Diclofenac and indomethacin treatment decreased cell growth by inducing cell cycle arrest and apoptosis. In addition, diclofenac and indomethacin reduced tumor volume in a xenograft model of ovarian cancer. To identify possible molecular pathways mediating the effects of NSAID treatment in ovarian cancer, we performed microarray analysis of ovarian cancer cells treated with indomethacin or diclofenac. Interestingly, several of the genes found downregulated following diclofenac or indomethacin treatment are transcriptional target genes of E2F1. E2F1 was downregulated at the mRNA and protein level upon treatment with diclofenac and indomethacin, and overexpression of E2F1 rescued cells from the growth inhibitory effects of diclofenac and indomethacin. In conclusion, NSAIDs diclofenac and indomethacin exert an anti-proliferative effect in ovarian cancer in vitro and in vivo and the effects of NSAIDs may be mediated, in part, by downregulation of E2F1.

2014-06-20 | GSE45052 | GEO

Non-steroidal Anti-inflammatory Drugs Decrease E2F1 Expression and Inhibit Cell Growth in Ovarian Cancer Cells

2014-06-20 | E-GEOD-45052 | biostudies-arrayexpress

Effect of ibuprofen on hippocampal gene expression in APP-PS1 mice

Project description:NSAIDs (non-steroidal anti-inflammatory drugs) inhibit cyclooxygenase (COX) enzymes and prevent Alzheimer’s disease (AD) at preclinical stages in cognitively normal aging populations. We modeled NSAID prevention of memory impairment in AD model mice to identify novel targets of NSAID action. We found that the widely-used NSAID ibuprofen prevented early hippocampus-dependent memory deficits in APP-PS1 mice. We therefore analyzed gene expression in the hippocampus of these mice.

2016-06-14 | GSE67306 | GEO

Gene expression of disseminated neuroblastoma

Project description:Comprehensive expression profiling of disseminated neuroblastoma with favorable and unfavorable outcome using SAGE. Results provide insight into the molecular pathogenesis of spontaneous regression and progression of metastatic neuroblastoma and may be used for improving risk estimation of patients with disseminated neuroblastoma. Keywords: gene expression SAGE-based, neuroblastoma, primary tumor, disseminated disease Samples analyzed: 9 (stage 4S neuroblastoma: n=5, stage 4 neuroblastoma: n=3, neuroblastoma cell line: n=1)

2006-09-06 | E-GEOD-4991 | biostudies-arrayexpress

Sirtuin 3 is a common target of non-steroidal anti-inflammatory drugs to induce gastric cancer cell death and gastric mucosal injury II.

Project description:Nonsteroidal anti-inflammatory drugs (NSAIDs), the quintessential medicines to treat pain and inflammatory conditions, induce cell death in human cancer cells, as repurposed anticancer agents, and in normal gastric mucosa, as a major side effect. The subcellular target/s of NSAIDs that leads to the cell death remained elusive so far. Here, by venturing transcriptomics followed by functional validation, we, for the first time, identified mitochondrial deacetylase Sirtuin 3 (Sirt3) as a non-canonical target of NSAIDs whose depletion induced the hyperacetylation of mitochondrial proteome, OGG1 depletion, mtDNA damage, electron transport chain defect associated mitochondrial dysfunction and finally cell death. Silencing of Sirt3 in AGS cells (a human gastric adenocarcinoma cell line) significantly aggravated NSAID-induced cytopathology. Whereas, honokiol mediated induction of Sirt3 corrected the NSAID-induced transcriptome alteration and gastropathy in rodent model. Together, the results identify Sirt3 as a common target used by NSAIDs to induce gastric carcinoma cell death and gastric mucosal injury.

2022-11-14 | GSE202140 | GEO

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