Effect of cholestasis on Dynamin-Related Protein 1 (Drp1) gene expression in rat liver
Journal Title: مجله علمي دانشگاه علوم پزشكي كردستان - Year 2017, Vol 22, Issue 90
Abstract
Background and Aim: Cholestasis is characterized by impaired bile flow, which can cause accumulation of bile acids in the liver and development of metabolic disorders, resulting in hepatocellular necrosis and apoptosis. Mitochondria are a critical cellular organelle that produces most of the cellular energy. Mitochondrial morphology varies from an interconnected filamentous network to isolated dots. This processes are called mitochondrial fission and fusion. Disrupted mitochondrial morphology has been observed in cholestatic liver disease. Dynamin related protein 1 is one of the genes involved in mitochondrial fission and plays a role in apoptosis. In this study we investigated Drp1 gene expression in the liver of cholestatic rats. Materials and Methods: In this experimental study, male Wistar rats (290±25g) were divided into three groups of control (non-operated), sham (operated without common bile duct ligation) and BDL (operated with common bile duct ligation). On the 28th day of BDL, rats were weighed and sacrificed. Biochemical assays for measurement of bilirubin level and liver enzymes, and also dissection of liver tissue for histopathological analysis were performed. Drp1 gene expression was evaluated by semi-quantitative RT-PCR technique. Results: The results showed that serum levels of total bilirubin and liver enzymes (ALT, AST, ALK) were significantly increased in BDL group compared to those in the control and sham operation groups (P<0.0001 and P<0.001). Histological examination revealed bile ductular hyperplasia, focal liver necrosis and fibrous tissue expansion in BDL group. The result of RT-PCR indicated significant increase of Drp1 gene expression in the liver of the rats in BDL group compared to that in the other groups (P<0.001). Conclusion: In this study we found that liver cholestasis increased expression of Drp1 gene which led to increased mitochondrial-mediated apoptotic effect with resultant liver cell death.
Authors and Affiliations
PhD F Khosrobakhsh, PhD M. R Moloudi, MSc M Bigdelo, MSc A Rahimmi
Keywords
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