Project description:Liver fibrosis is a common pathological complication of end-stage liver disease, which is usually associated with chronic liver inflammation and injury. Liver fibrosis was induced by bile duct ligation (BDL) in rats. The differentially expressed genes in liver tissue of BDL rats were identified by microarray technique.
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.
Project description:The aim is to characterize rat liver fibrosis induced by thioacetamide (TAA). To induce hepatic fibrosis, Male Sprague Dawley rats (9-12 weeks of age and 380-420 g of weight upon arrival, supplied by Beijing Vital River laboratory animal Co., Ltd.) were treated with thioacetamide (TAA). Rat liver samples were collected from five groups of rats at week 1, 2, 4, 8 and 13 after TAA (300 mg/kg) administration three times per week while five control groups receive the same volume of 0.9% normal saline. Four biological replicates were used for each group.
Project description:The aim is to characterize rat liver fibrosis induced by bile duct ligation (BDL). To induce hepatic fibrosis, Male Sprague Dawley rats (9-12 weeks of age and 380-420 g of weight upon arrival, supplied by Beijing Vital River laboratory animal Co., Ltd.) underwent surgery of bile duct ligation (BDL). The bile ducts of Sprague-Dawley rats were ligated after 12 hours of fasting and water deprivation. Rat liver samples were collected from three groups of rats at week 1, 2 and 5 after BDL surgery. Three control groups of rats underwent sham operation, including bile duct mobilization, but without BDL. Three biological replicates were used for each group.
Project description:Objective: To identify the long noncoding (lncRNA) and its potential roles in hepatic fibrosis rat liver issues induced by CCl4. Methods: LncRNAs and genes were analyzed in fibrosis rat liver issues by RNA sequencing and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Differential expressed lncRNAs and genes were subjected to bioinformatics analysis and involved to construct co-expression network.
Project description:A differential label-fee proteomics approach was performed using 27 biopsies from patients with HCV-associated hepatic fibrosis. For statistical analysis the patients were grouped into a low and a high fibrosis group. The low fibrosis group contained 13 patients of fibrosis stages 0, 1 and 2, whereas the high fibrosis group contained 14 patients of fibrosis stages 3 and 4 (fibrosis stages according to Batts-Ludwig classification).
Project description:Chronic activation of hepatic stellate cells leads to irreversible liver fibrosis, and durable treatment options for liver fibrosis remain suboptimal, creating a critical clinical need. Amniotic fluid (AF) reduces inflammation and promotes tissue remodeling and regeneration when applied to cutaneous wounds and in models thereof. However, no prior studies have explored the anti-fibrotic benefits of AF in liver disease. Data from this study indicate that AF can repress liver fibrosis by reducing hepatic stellate cell myofibroblast activation. Thus, these findings lay the foundation for early-phase clinical trials investigating cell-free AF as a therapeutic treatment for liver fibrosis and as a bridging therapy for liver transplantation
Project description:The experiment was to identify gene expression changes in mouse liver macrophages upon resolution from inflammation.<br>Macrophages were isolated from mouse livers 24 hours (inflammation) and 72 hours (resolution) following injury (hepatic fibrosis).<br>RNAs were prepared and hybrised on Affymetrix Mouse Genome 1.0 ST arrays.
Project description:Liver fibrosis is a strong predictor of long-term mortality in patients with non-alcoholic fatty liver disease; yet the mechanisms underlying the progression from the comparatively benign fatty liver state to advanced non-alcoholic steatohepatitis (NASH) and liver fibrosis are incompletely under-stood. Using a cell type-resolved genomics approach, we show that comprehensive alterations in hepatocyte genomic and transcriptional settings during NASH progression, led to a partial loss of hepatocyte identity. The hepatocyte reprogramming was under tight cooperative control of a net-work of NASH-activated transcription factors (TFs), as exemplified by Elf3 and Glis2. Indeed, Elf3 and Glis2 controlled hepatocyte identity and fibrosis-dependent hepatokine genes targeting disease-associated hepatic stellate cell (HSC) gene programs. Thus, interconnected TF networks not only promoted hepatocyte dysfunction, but also directed the intra-hepatic crosstalk with HSCs necessary for NASH and fibrosis progression implying molecular “hub-centered” targeting strategies to be superior to existing mono-target approaches as currently used in NASH therapy.