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Differential expression profile of liver fibrosis rats induced by CCl4

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE189402 | GEO | 2021/11/25

REPOSITORIES: GEO

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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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Aberrant expression of microRNAs is associated to the progression of liver fibrosis

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Carbon tetrachloride (CCl4) induced liver fibrosis

Project description:To understand the fibrotic response in the CCl4 induced liver fibrosis model, we performed RNA-seq of liver samples from mice treated with oil or CCl4.

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

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The Genetic Architecture of CCl4-induced Liver Fibrosis in Mice

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MiR-29a regulates liver fibrosis

Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been obserbed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis.

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Differential expression profile of liver fibrosis rats induced by CCl4

Project description:Differential expression profile of liver fibrosis rats induced by CCl4

| PRJNA782907 | ENA

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.

2021-02-02 | GSE110096 | GEO

Expression data that were specifically regulated by lncRNA-HELF (ENSMUST00000147617 ) in livers of mice undergoing CCl4-induced liver fibrosis

Project description:Long non-coding RNAs (lncRNAs) are involved in numerous biological functions and pathological processes. In this study, we have identified a novel lncRNA ENSMUST00000147617, named Highly Expressed in Liver Fibrosis (lnc-HELF), which is remarkably up-regulated in mouse and human fibrotic livers. To identify the roles of lnc-HELF in liver fibrosis, we performed RNA-seq to analyze the effect of lnc-HELF deficient on CCl4-induced liver fibrosis. The mice were divided in three groups: mice treated with CCl4 in combination with injection of AAV8-NC (NC_CCl4, n=3), mice treated with CCl4 in combination with injection of AAV8-shRNA-lncHELF1# (sh1_CCl4, n=3) and mice treated with CCl4 in combination with injection of AAV8-shRNA-lncHELF2# (sh2_CCl4, n=3).

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RNA sequencing of WT and Hmgb2-/- mice liver treated with CCL4

Project description:loss of Hmgb2 in vivo in mouse liver largely prevented CCl4-induced liver fibrosis. The goal of the RNA-seq is to identify the Hmgb2 regulated genes in CCL4 induced liver fibrosis.

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