Ontology highlight
ABSTRACT:
PROVIDER: PRJNA874684 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21292646_1.fastq.gz | Fastqsanger.gz | |||
| SRR21292646_2.fastq.gz | Fastqsanger.gz | |||
| SRR21292647_1.fastq.gz | Fastqsanger.gz | |||
| SRR21292647_2.fastq.gz | Fastqsanger.gz | |||
| SRR21292648_1.fastq.gz | Fastqsanger.gz |
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Project description:Background and Aims: The impact of cigarette smoke on inflammatory bowel disease has been established by a large number of epidemiological, clinical, and preclinical studies. Exposure to cigarette smoke is associated with a higher risk of developing Crohn’s disease but is inversely correlated with the development, disease risks, progression, and relapse rate of ulcerative colitis. Few mechanistic studies have investigated the effect of cigarette smoke on intestinal inflammation and microbial composition. Methods: Three groups of mice were exposed to three different concentrations of cigarette smoke for a total of 4 weeks, including 5 days of dextran sulfate sodium treatment to induce colitis and a 7-day recovery period. A comprehensive and integrated comparative analysis of the global colon transcriptome and microbiome, as well as classical endpoints, was performed. Results: Cigarette smoke exposure significantly decreased the severity induced colitis. Colon transcriptome analysis revealed that cigarette smoke downregulated specific pathways in a concentration-dependent manner, affecting both the inflammatory state and composition of the gut microbiome. Metagenomics analysis demonstrated that cigarette smoke can modulate dextran sulfate sodium-induced dysbiosis of specific bacterial genera, contributing to resolve the inflammation or accelerate recovery. Conclusions: Cigarette smoke alters gut microbial composition and reduces inflammatory responses in a concentration-dependent manner. The present study lays the foundation for investigating potential molecular mechanisms responsible for the attenuation of colitis by cigarette smoke.
2020-03-03 | E-MTAB-7988 | biostudies-arrayexpress
Project description:Oligo-fucoidan (OF), a sulfated polysaccharide extracted from brown seaweed, exhibits anti-inflammation and antitumor effects, however, knowledge concerning the detailed mechanism of oligo-fucoidan on liver cells is obscure. In this study, we investigate the effect of oligo-fucoidan in normal hepatocytes using transcriptomic analysis. Using an oligo-fucoidan oral gavage in adult wild-type zebrafish, we then used microarrays to detail the global programme of gene expression after fucoidan treatment and identified distinct classes of up- and down-regulated genes during this process.
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Project description:Fucoidan is a high-molecular polysaccharide whose main constituent is sulfated fucose. Extensive studies have demonstrated numerous interesting biological activities for fucoidan. We specifically focused on the anti-proliferation activity of fucoidan and examined the underlying mechanism in MKN45 gastric cancer cells. BrdU assay revealed that fucoidan impeded the MKN45 cell cycle by approximately 50%, and clonogenic assay also showed that fucoidan inhibited cell proliferation. Preliminary examinations of fucoidan using LDH assay showed no immediate cytotoxic effects at 24-h exposure. However, longer time courses revealed inhibition of cell growth at 4 days in a dose-dependent manner. Microarray analysis in MKN45 cells treated with fucoidan identified genes that were upregulated and downregulated in response to fucoidan, including MAP3K5, or ASK1 (apoptosis signal-regulating kinase), which was upregulated by 1.38-fold. Western blot confirmed that fucoidan increased ASK1 protein levels, while reducing the levels of phosphorylated ASK1. Reduction of ASK1 by siRNA decreased proliferation of MKN45 cells. Our findings show that fucoidan may suppress cellular proliferation and DNA synthesis in MKN45 cells by suppressing the ASK1-p38 signaling pathway through reduction of phosphorylated ASK1 levels.
2017-02-09 | GSE58774 | GEO
Project description:Hepatocellular carcinoma is the fourth leading cause of cancer-related deaths worldwide. Many carcinogens induce inflammation and cirrhosis, and eventually develop into liver cancer. Fucoidan is sulfated polysaccharide that is mainly found in brown seaweeds. In this study, we investigated the effects and mechanisms of low molecular weight fucoidan (i.e. oligo-fucoidan) preventing hepatocarcinogenesis using HBx,Src, and HBx,Src,p53-/+ transgenic zebrafish liver cancer model. Using an oligo-fucoidan oral gavage in adult transgenic zebrafish, we then used microarrays to detail the global programme of gene expression after fucoidan treatment and identified distinct classes of up- and down-regulated genes during this process.
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Project description:Fucoidan, a sulfated polysaccharide extracted from brown seaweeds, possesses many biological activities including anti-inflammatory and anti-oxidant activities. We aimed to investigate the protective effects of fucoidan on dyslipidemia and atherosclerosis in apolipoprotein E-deficient mice (ApoEshl mice) and to elucidate its molecular targets in the liver by using a transcriptomic approach. For 12 weeks, ApoEshl mice were fed a high-fat diet (HFD) supplemented with either 1% or 5% fucoidan. Fucoidan supplementation significantly reduced tissue weight (liver and white adipose tissue), blood lipid, total-cholesterol (TC), triglyceride (TG), non-high density lipoprotein-cholesterol (Non-HDL-C), and glucose levels in HFD-fed ApoEshl mice but increased plasma lipoprotein lipase (LPL) activity and HDL-C levels. Fucoidan also reduced hepatic steatosis levels (liver size, TC and TG levels, and lipid peroxidation) and increased white adipose tissue LPL activity. DNA microarray analysis and quantitative reverse transcription-polymerase chain reaction demonstrated differential expression of genes encoding proteins involved in lipid metabolism, energy homeostasis, and insulin sensitivity, by activating Ppara and inactivating Srebf1. Fucoidan supplementation markedly reduced the thickness of the lipid-rich plaque, lipid peroxidation, and foaming macrophage accumulation in the aorta in HFD-fed ApoEshl mice. Thus, fucoidan supplementation appears to have anti-dyslipidemic and anti-atherosclerotic effects by inducing LPL activity and inhibiting the effects of inflammation and oxidative stress in HFD-fed ApoEshl mice.
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Project description:Radiotherapy (RT) often causes unwanted side effects such as radiation-induced fibrosis (RIF) and second malignancies (SM). Fucoidan, a sulfated polysaccharide extracted from brown seaweed, has many biological effects including anti-inflammation and anti-tumor. In the present study, we investigated the radioprotective effect of Oligo-Fucoidan (OF) using zebrafish animal model. Using an oligo-fucoidan oral gavage in wild-type and adult transgenic zebrafish, we then used microarrays to detail the global programme of gene expression after fucoidan treatment and identified distinct classes of up- and down-regulated genes during this process.
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