Aim & Background: Cholestasis is characterized by impaired bile flow, which leads to accumulation of bile acids within liver and in the serum. Hydrophobic bile acids may cause hepatocellular necrosis and apoptosis during cholestatic liver diseases. Mitochondria are critical cellular organelles that produce most of the cellular energy. Mitochondrial morphology varies from an interconnected filamentous network to isolated dots. These processes are called mitochondrial fission and fusion. Disrupted mitochondrial morphology has been observed in cholestatic liver disease. MFN1 is the main molecule that regulates mitochondrial fusion and plays an important role in maintaining the homeostasis of mitochondrial morphology. It facilitates the binding of mitochondria in the early stage of the fusion. Mfn1 gene expression in the liver of cholestatic rats were examined in this study. Materials and Methods: The Male Wistar rats (280-340g) were used into three groups of control (nonoperated), sham (operated without common bile duct ligation) and BDL (operated with common bile duct ligation). On day 28 of BDL, rats were weighed and sacrificed. Biochemical assays and dissection of liver tissue for histopathological analysis and Mfn1 gene expression evaluation by semi-quantitative RT-PCR technique were performed. Results: The results revealed that serum levels of total Bilirubin and liver enzymes (ALT, AST,ALK) were significantly increased in BDL group as compared with the control and sham operation groups (P<0.01). Concerning histology, the appearance of biliary ductular hyperplasia, periductular inflammation and focal hepatocyte necrosis were noted with BDL group. The result also showed that the Mfn1 gene expression in liver of BDL rats significantly changed as compared with other groups (P<0.001). Conclusion: Our results suggest that change in balance of mitochondrial dynamics could participate in pathogenesis of cholestatic liver injury.
