Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA292840 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The study determined whether there were gender differences in the <br>expression of hippocampal genes in adult rats in association with dissimilarity <br>in their behavior, and how these were affected by prenatal stress. Pregnant <br>Wistar rats were subjected to varied stress once daily on days 14-20 of <br>gestation.<br>
2010-01-01 | E-MEXP-2470 | biostudies-arrayexpress
Project description:Psychological, psychosocial and physical stress are major risk factors, which enhance the development of sporadic late-onset Alzheimer`s disease. The chronic unpredictable mild stress model mimics those risk factors and triggers signs of neurodegeneration and neuropathological features of sporadic AD such as tau hyperphosphorylation and enhanced amyloid beta generation. The study investigated the impact of chronic unpredictable mild stress on signs of neurodegeneration by analyzing hippocampal gene expression with whole genome microarray gene expression profiling.
2015-08-13 | GSE72062 | GEO
Project description:Metronidazole and ciprofloxacin differentially affect chronic unpredictable mild stress-induced changes in colon, cecum and ileum microbiome
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Project description:Expression data from Chronic Unpredict Mild Stress-induced depression in GK rats‘ liver
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Project description:In this study we employed the chronic unpredictable stress (CUS) rat model that leads to anxiety features comparable to humans and validated in several published reports as a well-characterized model of depression symptoms with high predictive validity. Cytokines and activated intracellular kinase levels were determined using high throughput multiplex assays. RNA from freshly isolated adipocytes was used to run whole genome expression microarray profiling in control and stressed rats. Adipocyte function was assessed via tritiated glucose uptake assay. The expression of four cytokines (TNFα, IL-1β, IL-6 and MCP-1) was validated via real-time PCR and the all showed increased expression levels with chronic unpredictable stress. Male rats were subjected to chronic unpredictable stress for 35 days and total body fat was measured. The analyses presented here represents data from experiments performed in 6 control and 6 stressed rats in parallel. All cells for RNA isolation were collected at the conclusion of the 35 day stress protocol.
2014-06-03 | E-GEOD-47754 | biostudies-arrayexpress
Project description:Male Sprague-Dawley rats were used to establish exhausted-exercise model by motorized rodent treadmill. Yu-Ping-Feng-San at doses of 2.18 g/kg was administrated by gavage before exercise training for 10 consecutive days. Quantitative proteomics was performed for assessing the related mechanism of Yu-Ping-Feng-San.
2022-08-12 | PXD032737 | Pride
Project description:Major depression is a multidimensional disorder highly prevalent in modern society. Although several classes of antidepressants (ADs) are currently available to treat depression, the effectiveness of treatment is still limited, as many patients do not show full remission; thus, there is a need to find better patients’ directed therapeutic strategies. Neuroplastic changes in several brain regions, namely in the hippocampal dentate gyrus (DG), are amongst the best correlates of depression and of ADs actions. In this study the targets and molecular mediators of chronic stress and of four ADs from different pharmacological classes (fluoxetine, imipramine, tianeptine and agomelatine) were investigated in the DG. Using the unpredictable chronic mild stress (uCMS) animal model of depression, the molecular commonalities and specificities of the ADs were determined. All ADs, except agomelatine, could reverse the behavioral deficits produced by uCMS, and the neuroplastic changes in the DG; agomelatine reversed only the anhedonic profile in the sucrose consumption test. Chronic stress induced mild but relevant molecular changes that were mostly reversed by fluoxetine, imipramine and tianeptine. Fluoxetine reduced pro-inflammatory response and increased cell metabolism pathways. Its actions were mostly dependent on molecular changes occurring in neurons. Similarities were found between imipramine and tianeptine molecular actions and targets, as both activated pathways related to cellular protection. Moreover, no particular neural cell type enrichment was found with both treatments. Agomelatine presented a very dissimilar molecular pattern impacting greatly on Rho-GTPases-related pathways in oligodendrocytes and neurons. The recognition of these molecular alterations contributes to the understanding of the processes implicated in the onset and treatment of depression and may pave the way for more effective therapeutic interventions. We compared gene expresssion in the dentate gyros of rats which were either untreated, exposed to unpredictable chronic mild stress, or exposed to the same stress and treated with either fluoxetine, imipramine, tianeptine, or agomelatine
2015-07-02 | E-GEOD-56028 | biostudies-arrayexpress
Project description:Right ventricular heart failure (RVF) associated with pulmonary hypertension (PH) is characterized by a distinct gene expression pattern when compared with functional compensatory hypertrophy. Carvedilol treatment after RVF has been established reduces right ventricle (RV) hypertrophy and improves the RV function. In addition, carvedilol treatment has been shown to alter the gene expression of select genes. We sought to identify, on a genome-wide basis, the effect of carvedilol on gene expression. RVF was induced in male Sprague-Dawley rats by the combination of VEGF-receptor blockade and chronic hypoxia; thereafter, one group was treated with carvedilol. RNA was isolated from the RV and subjected to microarray analysis. A prediction analysis of the carvedilol-treated RVs showed that carvedilol treated RVs most resembled in their expression pattern the RVF pattern. However, an analysis beyond the boundaries of the prediction set revealed a small set of genes associated with carvedilol reversal of RVF. Pathway analysis of this set of genes revealed expression changes of genes involved in cardiac hypertrophy, mitochondrial dysfunction, protein ubiquitination, and sphingolipid metabolism. Genes encoding proteins in the cardiac hypertrophy and protein ubiquitination pathways were downregulated in the RV by carvedilol, while genes encoding proteins in the mitochondrial dysfunction and sphingolipid metabolism pathways were upregulated by carvedilol.
2013-05-06 | GSE42579 | GEO