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  • 1
    Online Resource
    Online Resource
    Wiley ; 2016
    In:  Journal of Digestive Diseases Vol. 17, No. 11 ( 2016-11), p. 756-763
    In: Journal of Digestive Diseases, Wiley, Vol. 17, No. 11 ( 2016-11), p. 756-763
    Abstract: Although the intimate relationship between liver and gut has been previously reported under physiological and pathological conditions, intestinal involvement in the process of intrahepatic cholestasis of pregnancy remains unclear. The aim of this study was to investigate intestinal changes in 17α‐ethynylestradiol (EE)‐induced cholestatic rat model. Methods Liver injury was assessed by HE stain and serum biochemical parameters were measured. Intestinal transit was determined using ink marks. Neuronal protein expressions in the intestine were analyzed by Western blot. Results EE treatment induced liver damage, including severe bile duct hyperplasia, portal edema, portal infiltration, a loss of hepatic structure in periportal areas and increased serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and total bilirubin. Large areas of inflammatory cell infiltration and increased myeloperoxidase activity were observed in the intestine of EE‐induced cholestatic rats. The EE‐treated group showed increased intestinal transit and malondialdehyde levels, while the glutathione content and superoxide dismutase activity were notably decreased, together with decreased protein gene product 9.5 and neuronal nitric oxide synthase expression in the ileum and colon. Furthermore, choline acetyltransferase expression was significantly decreased in the ileum, whereas no change was observed in the colon of EE‐treated rats. Conclusion EE‐induced liver damage is associated with oxidative stress, inflammation and neural loss in the intestine, which may lead to altered intestinal motility.
    Type of Medium: Online Resource
    ISSN: 1751-2972 , 1751-2980
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2317117-0
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