Project description:Intoxication with CCl4 is a frequently used technique to induce liver damage in mice. The compound induces cell death of hepatocytes in the pericentral region of the liver lobule.
Project description:Male C57BL6/N mice were obtained from Janvier Labs (France). Mice were starved overnight before APAP administration and were fed ad libitum afterward. A single dose of 300 mg APAP/kg b.w. was intraperitoneally injected in warm phosphate-buffered saline (PBS; Table 3). The used APAP was obtained from Sigma-Aldrich (A7085-500G, Germany). The mice were sacrificed at 1, 6, and 12 hours, and on days 1, 2, 4, 6, and 8 after APAP administration. Expression data of the livers of male C57Bl6/N mice after intoxication with paracetamol (APAP)
Project description:Lipopolysaccharides (LPS) are found in the outer membrane of Gram-negative bacteria. The intraperitoneal (i.p.) application of LPS into mice represents a frequently applied experimental model to induce hepatic and systemic inflammation.
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.
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).
Project description:Hepatic stellate cells are involved in the development of hepatic fibrosis. We here perform transcriptional profiling of hepatic stellate cells (HSCs) isolated from Western diet/high fructose-fed C57BL6/J mice, carbon tretrachloride (CCl4)-treated C57BL6/J mice, and of murine HSCs differentiated in vitro. Specifically, gene expression profiles are obtained from hepatic stellate cells isolated from C57BL6 mice fed a Western Diet supplemented with high fructose for 12, 16 or 24 weeks or normal chow. From hepatic stellate cells isolated from C57BL6 mice treated CCl4 for 1, 4 or 8 weeks or treated with vehicle. From hepatic stellate cells isolated from healthy C57BL6 mice and seeded on normal plastic cell culture dishes for 1, 4, 8, or 12 days. And from hepatic stellate cells isolated from healthy C57BL6 mice and seeded on normal plastic cell culture dishes for 6 days in the presence of 10uM U0126 or DMSO.
Project description:To investigate the altered gene expression levels in mouse fibrotic liver tissues, C57BL6/J mice were intraperitoneally injected with CCl4 or vehicle twice every week. After 8 weeks, livers were harvested and RNA was extracted by Trizol. The gene expression levels were analyzed and compared between CCl4 treated group and vehicle treated (control) group.
Project description:Long noncoding RNAs (lncRNAs) play important roles in various biological processes; however, few have been identified that regulate hepatic stellate cells (HSCs) activation and the progression of liver fibrosis. Through a detailed analysis of the expression of lncRNAs in various tissues, we discovered the existence of a liver enriched lncRNA-LFAR1 (lncRNA-Liver Fibrosis Associated RNA1). To identify the roles of lncRNA-LFAR1 in liver fiboris, we systematically analyzed the regulation of mRNAs in the livers of mice treated with oil in combination with injection of Lenti-NC (NC, n=3), CCl4 in combination with injection of Lenti-NC (NC+CCl4, n=3), oil in combination with injection of Lenti-shLFAR1 (shLFAR1, n=3) and CCl4 in combination with injection of Lenti-shLFAR1 (shLFAR1+CCl4, n=3) by mRNA microarrays, which revealed a panel of mRNAs that were specifically regulated by lncRNA-LFAR1 in livers of mice undergoing hepatic fibrosis. To identify the roles of lncRNAs-LFAR1 in regulating liver fiboris and the potential targets of lncRNA-LFAR1 in liver fiboris,we determined the mRNA expression profiles in the livers of Balb/c mice treated with oil in combination with injection of Lenti-NC (NC, n=3), CCl4 in combination with injection of Lenti-NC (NC+CCl4, n=3), oil in combination with injection of Lenti-shLFAR1 (shLFAR1, n=3) and CCl4 in combination with injection of Lenti-shLFAR1 (shLFAR1+CCl4, n=3) by mRNA microarrays.