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BDL-Induced Liver Fibrosis / Cirrhosis

Liver fibrosis results from chronic injury such as that caused by viral hepatitis (especially hepatitis B and C), alcohol abuse, drugs, metabolic diseases due to overload of iron or copper, congenital abnormalities or autoimmune attack of hepatocytes or bile duct epithelium. It is characterized by the encapsulation or replacement of injured tissue by a collagenous scar. Liver fibrosis is reversible, whereas cirrhosis, the later stage of fibrosis progression, featuring regenerative nodules surrounded by fibrous bands, is generally irreversible. Liver cirrhosis leads to impaired liver function with increased intrahepatic resistance (portal hypertension) and increased risk of hepatocellular carcinoma (HCC).

Bile Duct Ligation (BDL) induced liver fibrosis / cirrhosis in rodents is a well-established and widely accepted experimental model for the study of liver fibrosis and cirrhosis. This model has similar histological, biochemical, cellular and molecular changes associated with hepatic fibrosis.

PharmaLegacy Models and Research Tools

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Case: BDL-induced liver fibrosis/ cirrhosis in rats
BDL-induced liver cirrhosis: Group and Surgical Regimen


BDL-induced liver cirrhosis: Hepatic Hydroxyproline (HYP) Content quantitation

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BDL-induced liver cirrhosis: BDL Liver Histology (H&E Staining)

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BDL-induced liver cirrhosis: BDL Liver Histology (H&E Staining)

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The morphological changes seen in the BDL model include bile duct proliferation, dilatation and infiltration of inflammatory cells. At week 7, most hepatic lobules were replaced by the proliferated bile ducts and fibrous tissue.


BDL-induced liver cirrhosis: BDL Liver Histology (Sirius red Staining)

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Hepatic fibrosis developed at week 1 after BDL, and increased in the following weeks. At week 7, portal-portal and portal-central were connected by fibrous tissue, and even hepatic lobules were replaced by fiber deposition.





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