- Volume 45 Issue 2
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Cell Death and Proliferation after Treatment and Reinfection of Clonorchis sinensis in the Sprague-Dawley Rat Bile Duct
- Min, Byoung-Hoon (Xenotransplantation Research Center, Seoul National University College of Medicine) ;
- Ahn, Ka-Young (Department of Parasitology and the Institute of Travel Medicine, Korea University College of Medicine) ;
- Lee, Haeng-Sook (Department of Parasitology and the Institute of Travel Medicine, Korea University College of Medicine) ;
- Kim, Soo-Jin (Department of Life Science, College of Natural Science, Hallym University) ;
- Joo, Kyoung-Hwan (Department of Parasitology and the Institute of Travel Medicine, Korea University College of Medicine)
- Received : 2015.04.14
- Accepted : 2015.05.13
- Published : 2015.06.30
The structural change and distribution of mitochondrial enzyme (ATPase, cytochrome-c-oxidase), cell proliferation (proliferating cell nuclear antigen, PCNA), cell death (caspase-3) and cell growth factor (fibroblast growth factor 8, FGF-8) in the Sprague-Dawley rat bile duct during Clonorchis sinensis infection was investigated. Experimental groups were divided into C. sinensis infection, superinfection and reinfection of C. sinensis after 'praziquantel' treatment group. As a result, C. sinensis infected rat bile ducts showed the features of chronic clonorchiasis, i.e., connective tissue thickening, ductal fibrosis and epithelial tissue dilatation. PCNA for cell proliferation increased in the infection group, and decreased after praziquantel treatment. Caspase-3 was distributed in reinfection group only. FGF-8 was distributed in the rat bile duct after praziquantel treatment but not distributed in infection and reinfection group. Overall, C. sinensis infection causes physical and chemical irritations and then brings on the abnormalities of intracellular energy metabolism and cellular growth factors, which hinders bile duct tissue from functioning properly, and resultingly, fibrosis occurs and epithelial cells dilated abnormally. More intense infection makes tissue fibrosis chronical and activates apoptosis factors.
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