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ABSTRACT: Effect of indobufen treatment on HFHC diet-induced MAPK activation and NASH in mice

PROVIDER: PRJNA1024665 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26299451.fastq.gz	Fastqsanger.gz
	SRR26299452.fastq.gz	Fastqsanger.gz
	SRR26299453.fastq.gz	Fastqsanger.gz
	SRR26299454.fastq.gz	Fastqsanger.gz
	SRR26299455.fastq.gz	Fastqsanger.gz

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Project description:Effect of indobufen treatment on HFHC diet-induced MAPK activation and NASH in Sike KO mice

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Effects of NAFLD/NASH on hepatic gene expression.

Project description:To characterize gene expression changes in arachidonic acid metabolism pathway genes in the presense of non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) mice administered were administered an atherogenic diet for a period of four weeks. Administration of the atherogenic diet resulted in significant enrichment of the arachidonic acid metabolism pathway by gene set enrichment analysis (GSEA). The core enrichment subset of genes was down-regulated in mice administered the atherogenic diet and the majority of the genes that were down-regulated were cytochrome P450s. A total of 4 wild-type mice were administered a standard diet (STD; control group) and 4 wild-type mice were administered a HFHC diet (HFHC).

2014-01-03 | E-GEOD-53381 | biostudies-arrayexpress

Dietary cholesterol promotes fatty liver-associated liver cancer by inducing aberrant genomic expression and mutations

Project description:We investigated the effects of cholesterol on nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) in diethylnitrosamine-injected mice fed high-fat high-cholesterol (HFHC) diet versus high-fat (HF) alone. mRNA microarray analysis was applied for expressional aberrations.

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Project description:In our study, C57BL/6 male mice were fed a normal chow diet or high-fat diet additionally containing high-fructose and high-cholesterol (HFHC diet) for 12 weeks and 28 weeks to construct simple steatosis (NAFL) and Non-alcoholic steatohepatitis (NASH) models respectively. Through miRNA sequencing, 420 miRNAs were detected. A total of 148 miRNAs (14 up-regulated and 34 down-regulated) and 146 miRNAs (74 up-regulated and 72 down-regulated) were differentially expressed in livers of NAFL and NASH mice, respectively. A total of 36 miRNAs (8 up-regulated; 28 down-regulated) were dysregulated in both NASH and NAFL mice, while 110 miRNAs (66 up-regulated; 44 down-regulated) were altered specifically in NASH mice.

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Changes of hepatic gene expression in C57BL/6N male mice fed high-fat high-calorie fructose (HFHC) diet for 8 weeks

Project description:In murine NAFL/NASH models, high-fat high-calorie fructose (HFHC) diet fed for 16 weeks induces hepatic steatosis, inflammatory cells infilatration and early stage fibrosis. In addition, HFHC diet 16 weeks but not 8 weeks is accompanied with weight gain and insulin resistance. The aim of this study is to determine the gene expression changes in mouse liver by HFHC diet for 8weeks.

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Project description:Effect of sorafenib on high fat high cholesterol (HFHC) diet induced NASH in mice

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M-NM-2-Cryptoxanthin suppresses inflammatory gene expression in diet-induced nonalcoholic steatohepatitis in mice

Project description:To evaluate the effect of M-NM-2-cryptoxanthin on diet-induced NASH, we fed a high-cholesterol and high-fat diet (CL diet) with or without 0.003% M-NM-2-cryptoxanthin to C56BL/6J mice for 12 weeks. After feeding, M-NM-2-cryptoxanthin attenuated fat accumulation, increases in Kupffer and activated stellate cells, and fibrosis in CL diet-induced NASH in the mice. Comprehensive gene expression analysis showed that although M-NM-2-cryptoxanthin histochemically reduced steatosis, it was more effective in inhibiting inflammatory gene expression change in NASH. M-NM-2-Cryptoxanthin reduced the alteration of expression of genes associated with cell death, inflammatory responses, infiltration and activation of macrophages and other leukocytes, quantity of T cells, and free radical scavenging. However, it showed little effect on the expression of genes related to cholesterol and other lipid metabolism. The expression of markers of M1 and M2 macrophages, T helper cells, and cytotoxic T cells was significantly induced in NASH and reduced by M-NM-2-cryptoxanthin. M-NM-2-Cryptoxanthin suppressed the expression of lipopolysaccharide (LPS)-inducible and/or TNFM-NM-1-inducible genes and the antioxidant enzyme glutathione peroxidase 1 in NASH. Thus, M-NM-2-cryptoxanthin suppresses inflammation and the resulting fibrosis probably by primarily suppressing the increase and activation of macrophages and other immune cells. Reducing oxidative stress is likely to be a major mechanism of inflammation and injury suppression in the livers of mice with NASH. Eight-week old male C57BL/6J mice were fed for 12 weeks on a CRF-1 standard chow (control), a high-cholesterol and high-fat diet (CL diet; 38.23% CRF-1, 60% cocoa butter, 1.25% cholesterol, 0.5% sodium cholate) or a CL diet containing 0.003% M-NM-2-cryptoxanthin.

2014-05-28 | E-GEOD-51432 | biostudies-arrayexpress

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