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Aanalysis transcriptomes of Schisandrin B alleviates CCl4-induced liver fibrosis in rats by RNA-sequencing

ABSTRACT: Aanalysis transcriptomes of Schisandrin B alleviates CCl4-induced liver fibrosis in rats by RNA-sequencing

PROVIDER: PRJNA432742 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6667830.fastq.gz	Fastqsanger.gz
	SRR6667831.fastq.gz	Fastqsanger.gz
	SRR6667832.fastq.gz	Fastqsanger.gz
	SRR6667833.fastq.gz	Fastqsanger.gz
	SRR6667834.fastq.gz	Fastqsanger.gz

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Aanalysis transcriptomes of Schisandrin B alleviates CCl4-induced liver fibrosis in rats by RNA-sequencing

Project description:Transcriptome analysis is an effective method to study a comprehensive understanding of molecular mechanisms involved in biological processes and diseases by RNA-Sequencing (RNA-Seq). This study aimed to elucidate the possible mechanisms of Schisandrin B on CCl4-induced liver fibrosis through detecteing hepatic gene expression profiles by RNA-Seq.

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Differential expression profile of liver fibrosis rats induced by CCl4

Project description:This study aimed to investigate the protective mechanisms of helenalin on hepatic fibrosis,Rats were intragastrically administrated with 50% CCl4 for 9 weeks to induce liver fibrosis, followed by various medicines for 6 weeks. The transcriptomic analysis was performed in liver tissues by RNA-seq.

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proteomics for CCL4-induced liver fibrosis

Project description:Proteomics for CCL4-induced liver fibrosis。 To understand the transcriptome data of liver fibrosis induced by CCl4 in mice. Methods: C57BL/6 mice were used to duplicate the liver fibrosis model induced by CCl-4. After successful replication, liver proteins were extracted from mice for subsequent experiments. Our experiment finally obtained protein data of CCL4-induced liver fibrosis model in mice, which provided further biological basis for our future study of liver fibrosis in mice.

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MicroRNA expression profiling of CCl4-induced liver fibrosis in Mus musculus

Project description:To investigate the differences in microRNA expression profiles between fibrotic and normal livers, we performed microRNA microarrays for total RNA extracts isolated from mouse livers treated with carbontetrachloride (CCl4) or corn-oil for 10 weeks (n=3/group). MicroRNAs were considered to have significant differences in expression level when the expression difference showed more than two-fold change between the experimental and control groups at p<0.05. We found that 12 miRNAs were differentially expressed in CCl4-induced fibrotic liver. To induce chronic liver fibrosis, seven-week-old mice received 0.6 ml/kg body weight of carbon-tetrachloride (CCl4) dissolved in corn-oil by intraperitoneal (i.p.) injection, twice a week for 10 weeks (n=3). As a control, same number of mice was injected with equal volume of corn-oil for 10 weeks.

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Transcriptomic profile of liver fibrosis in mice induced by CCl4

Project description:This study is aimed to investigate the underlying mechanisms of didymin on anti-hepatic fibrosis. In brief, mice were randomly devided into three groups,including normal, CCl4 and didymin groups. Except the normal group, mice were intra-peritonelly administrated with 20% CCl4 for 10 weeks to induce liver fibrosis; after modeling successfully, mice in didymin group were subsequently intragastrically administrated with didymin for 6 weeks. Finally, the transcriptomic analysis was performed to acquire the differently expressed genes amog the three groups, trying to figure out the potential targets, which regulated by didymin.

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Project description:Liver fibrosis is a multifactorial trait that develops in response to chronic liver injury. Our aim was to characterize the genetic architecture of carbon tetrachloride (CCl4)-induced liver fibrosis using the Hybrid Mouse Diversity Panel (HMDP), a panel of over 100 genetically distinct mouse strains optimized for genome wide association studies and systems genetics. Chronic liver injury was induced by CCl4 injections twice weekly for six weeks. 437 mice received CCl4 and 256 received vehicle, after which animals were sacrificed for liver histology and gene expression. Using automated digital image analysis, we quantified fibrosis as the collagen proportionate area % (CPA%) of the whole section, excluding normal collagen. We discovered broad variation in fibrosis among the HMDP strains, demonstrating a significant genetic influence on this trait, with an estimated heritability (H2) of 44%. Genome-wide association analyses revealed significant and suggestive loci underlying susceptibility to fibrosis, some of which overlapped with loci identified in mouse crosses and human population studies. Liver global gene expression was assessed by RNA sequencing, and gene set enrichment analyses identified the underlying pathways, of which stellate cell involvement was prominent. We also performed expression quantitative trait locus analyses to identify strong causal candidate genes. Our results provide a rich resource for the design of experiments to understand mechanisms underlying fibrosis and for rational strain selection when testing anti-fibrotic drugs.

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