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Research ArticleOriginal Article
Open Access

Hepatic oval cells activated by hepatocyte apoptosis in diethylnitrosamine-induced rat liver cirrhosis

Xi-Ming Xu, Guang-Jin Yuan, Jun-Jian Deng, Yao-Gui Wu, Wei Ge and Qi-Bing Song
Saudi Medical Journal May 2010, 31 (5) 490-494;
Xi-Ming Xu
Cancer Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China. Tel. +86 (27) 88041911. Fax. +86 (27) 88042292. E-mail: [email protected]
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Guang-Jin Yuan
Cancer Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China. Tel. +86 (27) 88041911. Fax. +86 (27) 88042292. E-mail: [email protected]
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Jun-Jian Deng
Cancer Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China. Tel. +86 (27) 88041911. Fax. +86 (27) 88042292. E-mail: [email protected]
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Yao-Gui Wu
Cancer Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China. Tel. +86 (27) 88041911. Fax. +86 (27) 88042292. E-mail: [email protected]
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Wei Ge
Cancer Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China. Tel. +86 (27) 88041911. Fax. +86 (27) 88042292. E-mail: [email protected]
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Qi-Bing Song
Cancer Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China. Tel. +86 (27) 88041911. Fax. +86 (27) 88042292. E-mail: [email protected]
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Abstract

OBJECTIVE: To investigate whether hepatic oval cells are activated in diethylnitrosamine (DEN)-induced rat liver cirrhosis, and to explore its mechanism.

METHODS: Liver cirrhosis was induced in rats (n=8) by weekly intraperitoneal injections of DEN at a dose of 50mg/kg body weight for 12 weeks followed by a 2-week wash out period. Rats (n=5) that received isovolumic vehicle served as the control group. Liver pathology was examined. Apoptotic hepatocytes were identified and quantified by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) assay. Oval cells were detected using immunohistochemical staining for pyruvate kinase type M2 (M2PK) and cytokeratin 19 (CK19). The work was carried out at Renmin Hospital of Wuhan University, Wuhan, Hubei, China from February to December 2009.

RESULTS: Liver cirrhosis developed in rats subjected to DEN administration. The TUNEL and morphology assay showed that a substantial number of hepatocytes underwent apoptosis. The apoptotic index in rats subjected to DEN administration (0.75 – 0.15) was much higher than normal control rats (0.10 – 0.05). Both CK19 and M2PK were moderately expressed in the rat liver cirrhosis, and the expression was dispersed or forming small cords in the liver; but the expression was hardly detected in the liver tissue of normal control rats.

CONCLUSION: In the DEN-induced rat liver cirrhosis, oval cells are activated and stimulated to proliferation, the mechanism of which may be related to substantial hepatocyte apoptosis in the model.

  • Copyright: © Saudi Medical Journal

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Saudi Medical Journal: 31 (5)
Saudi Medical Journal
Vol. 31, Issue 5
1 May 2010
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Hepatic oval cells activated by hepatocyte apoptosis in diethylnitrosamine-induced rat liver cirrhosis
Xi-Ming Xu, Guang-Jin Yuan, Jun-Jian Deng, Yao-Gui Wu, Wei Ge, Qi-Bing Song
Saudi Medical Journal May 2010, 31 (5) 490-494;

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Hepatic oval cells activated by hepatocyte apoptosis in diethylnitrosamine-induced rat liver cirrhosis
Xi-Ming Xu, Guang-Jin Yuan, Jun-Jian Deng, Yao-Gui Wu, Wei Ge, Qi-Bing Song
Saudi Medical Journal May 2010, 31 (5) 490-494;
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© 2025 Saudi Medical Journal Saudi Medical Journal is copyright under the Berne Convention and the International Copyright Convention.  Saudi Medical Journal is an Open Access journal and articles published are distributed under the terms of the Creative Commons Attribution-NonCommercial License (CC BY-NC). Readers may copy, distribute, and display the work for non-commercial purposes with the proper citation of the original work. Electronic ISSN 1658-3175. Print ISSN 0379-5284.

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