Pathological Lesions and Inducible Nitric Oxide Synthase Expressions in the Liver of Mice Experimentally Infected with Clonorchis sinensis

Qing-Li Yang; Ji-Qing Shen; Yan Xue; Xiao-Bing Cheng; Zhi-Hua Jiang; Yi-Chao Yang; Ying-Dan Chen; Xiao-Nong Zhou

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자료유형: 학술저널

저자정보: Qing-Li Yang (WHO Collaborating Centre for Malaria, Schistosomiasis and Filariasis) Ji-Qing Shen (Guangxi Medical University) Yan Xue (Guangxi Medical University) Xiao-Bing Cheng (Guangxi Medical University) Zhi-Hua Jiang (Guangxi Zhuang Autonomous Region Center for Disease Prevention and Control) Yi-Chao Yang (Guangxi Zhuang Autonomous Region Center for Disease Prevention and Control) Ying-Dan Chen (WHO Collaborating Centre for Malaria, Schistosomiasis and Filariasis) Xiao-Nong Zhou (WHO Collaborating Centre for Malaria, Schistosomiasis and Filariasis)

저널정보: 대한기생충학열대의학회 Parasites, Hosts and Diseases The Korean Journal of Parasitology Vol.53 No.6

발행연도: 2015.12

수록면: 777 - 783 (7page)

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The nitric oxide (NO) formation and intrinsic nitrosation may be involved in the possible mechanisms of liver fluke-associated carcinogenesis. We still do not know much about the responses of inducible NO synthase (iNOS) induced by Clonorchis sinensis infection. This study was conducted to explore the pathological lesions and iNOS expressions in the liver of mice with different infection intensity levels of C. sinensis. Extensive periductal inflammatory cell infiltration, bile duct hyperplasia, and fibrosis were commonly observed during the infection. The different pathological responses in liver tissues strongly correlated with the infection intensity of C. sinensis. Massive acute spotty necrosis occurred in the liver parenchyma after a severe infection. The iNOS activity in liver tissues increased, and iNOS-expressing cells with morphological differences were observed after a moderate or severe infection. The iNOS-expressing cells in liver tissues had multiple origins.

#Clonorchis sinensis #pathology #inducible nitric oxide synthase #liver #immunohistochemistry

참고문헌 (38)

참고문헌 신청

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