system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: UNLABELLED. Meshes: ATP Binding Cassette Transporter, Subfamily B, Animals, Cell Proliferation, Disease Progression, Extracellular Signal-Regulated MAP Kinases, Female, Heme Oxygenase-1, Liver Cirrhosis, Membrane Proteins, Mice, Mice, Knockout, Phosphorylation, Protoporphyrins, Receptors, Tumor Necrosis Factor.
user
Does induction of heme oxygenase 1 prevent progression of liver fibrosis in Mdr2 knockout mice? Context: Induction or overexpression of the heme-degrading enzyme, heme oxygenase 1 (HO-1), has been shown to protect mice from liver damage induced by acute inflammation. We have investigated the effects of HO-1 induction in a mouse model of chronic liver inflammation and fibrogenesis with progression to hepatocellular carcinoma (HCC) (Mdr2ko; FVB.129P2-Abcb4(tm1Bor)). HO-1 was induced in vivo by treatment with cobalt protoporphyrin IX, starting at week 5 or 12 of mice lifespan, and continued for 7 weeks. Our results showed that HO-1 induction reduced liver damage and chronic inflammation by regulating immune cell infiltration or proliferation as well as tumor necrosis factor receptor signaling. Fibrosis progression was significantly reduced by HO-1 induction in mice with mild, as well as established, portal and lobular fibrosis. HO-1 induction significantly suppressed hepatic stellate cell activation. During established fibrosis, HO-1 induction was able to revert portal inflammation and fibrosis below levels observed at the start of treatment. Moreover, hepatocellular proliferation and signs of dysplasia were decreased after HO-1 induction.
assistant
Induction of HO-1 interferes with chronic inflammation and fibrogenesis and, in consequence, might delay progression to HCC. Final Decision: yes