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:Background and aims: There are considerable evidences demonstrating that angiogenesis and chronic inflammation are mutually dependent. However, although cirrhosis progression is characterized with a chronic hepatic inflammatory process, this connection is not sufficiently explored as a therapeutic strategy. Therefore, this study was aimed to assess the potential benefits of targeting angiogenesis in cirrhotic livers to modulate inflammation and fibrosis. For this purpose, we evaluate the therapeutic utility of angiogenesis inhibitors. Methods: The in vivo effects of angiogenesis inhibitors were monitored in liver of cirrhotic rats by measuring angiogenesis, inflammatory infiltrate, fibrosis, a-smooth muscle actin (a-SMA) accumulation, differential gene expression (by microarrays), and portal pressure. Results: Cirrhosis progression was associated with a significant enhancement of vascular density and expression of vascular endothelial growth factor-A (VEGF-A), angiopoietin-1, angiopoietin-2 and placental growth factor (PlGF) in cirrhotic livers. The newly formed hepatic vasculature expressed vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Interestingly, the expression of these adhesion molecules correlated well with local inflammatory infiltrate. Livers of cirrhotic rats treated with angiogenesis inhibitors presented a significant decrease in hepatic vascular density, inflammatory infiltrate, a-SMA abundance, collagen expression and portal pressure. Conclusion: Angiogenesis inhibitors may offer a potential novel therapy for cirrhosis due to its multiple mechanisms of action against angiogenesis, inflammation and fibrosis in cirrhotic livers. Keywords: angiogenesis, cirrhosis, liver, Affymetrix, fibrosis