top of page
Acute-on-Chronic Liver Failure
Carbon tetrachloride (CCl4) + Ethanol - Act as agents to create chronic liver injury by inducing massive oxidative stress and hepatocyte necrosis and Acute insult (Lipopolysaccharide ) - Triggers a, massive systemic inflammatory response, activating TLR4 signaling and leading to acute, excessive production of pro-inflammatory cytokines 

Acute-on-Chronic Liver Failure

  • Genotype

    Carbon tetrachloride (CCl4) + Ethanol + Acute insult (Lipopolysaccharide )

  • Mechanism

    Carbon tetrachloride (CCl4) + Ethanol - Act as agents to create chronic liver injury by inducing massive oxidative stress and hepatocyte necrosis and Acute insult (Lipopolysaccharide ) - Triggers a, massive systemic inflammatory response, activating TLR4 signaling and leading to acute, excessive production of pro-inflammatory cytokines 

  • Phenotype

    Locomotor activity, Loss of equilibrium, Fatigue, Reduced feeding behavior

  • Biomarker

    ALT, AST, Bilirubin, Albumin, Ammonia

  • Gene Expression Markers

    tnfα, il1β, il6, nrf2, sod1, gpx1,srebp1, fasn, pparα, cyp2e1, gstp1 

  • Physiology Changes

    Hyperammonia, Oxidative stress, Metabolic dysregulation

  • Histology Grading Endpoint

    Hepatocellular necrosis, Ballooning degeneration, Steatosis, Fibrosis, Inflammatory cell infiltration

bottom of page