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实验诱导叙利亚仓鼠(金黄地鼠)双腔吸虫病所引起的形态学和生化变化

Morphologic and biochemical changes caused by experimentally induced dicroceliosis in hamsters (Mesocricetus auratus).

作者信息

Sánchez-Campos S, González P, Ferreras C, García-Iglesias M J, González-Gallego J, Tuñón M J

机构信息

Department of Physiology, University of León, Spain.

出版信息

Comp Med. 2000 Apr;50(2):147-52.

PMID:10857005
Abstract

BACKGROUND AND PURPOSE

The aim of the study reported here was to investigate the pathomorphologic changes caused by experimentally induced dicroceliosis and their correlation with hepatobiliary function.

METHODS

Studies were carried out at days 80 and 120 after oral inoculation of hamsters with 40 metacercariae of Dicrocoelium dendriticum.

RESULTS

The parasite-induced pathologic changes were assessed by presence of fluke eggs in feces, increased plasma alanine transaminase and aspartate transaminase activities and morphologic alterations. Dicroceliosis was characterized by bile ductular proliferation and enlargement of the bile duct surface area caused by hyperplastic cholangitis in septal bile ducts. The liver from infected animals contained portal tracts infiltrated with small to moderate numbers of lymphocytes, macrophages, and eosinophils. Simultaneously, there was an increase in portal tract collagen that extended to the interlobular septa and caused pressure atrophy of the hepatic parenchyma. The concentration of thiobarbituric acid-reactive substances and the ratio of oxidized to reduced glutathione, measured as markers of oxidative stress, were significantly increased.

CONCLUSIONS

The presence of oxidative alterations could be related to the morphologic evidence of chronic inflammatory response as well as to liver cellular injury indicated by cellular swelling, and increased presence of peroxisomes and lysosomes.

摘要

背景与目的

本文报道的这项研究旨在探究实验性诱发双腔吸虫病所导致的病理形态学变化及其与肝胆功能的相关性。

方法

在给仓鼠经口接种40个枝双腔吸虫囊蚴后的第80天和第120天开展研究。

结果

通过粪便中吸虫卵的存在、血浆丙氨酸转氨酶和天冬氨酸转氨酶活性升高以及形态学改变来评估寄生虫诱发的病理变化。双腔吸虫病的特征为胆管增生以及由间隔胆管的增生性胆管炎导致的胆管表面积增大。受感染动物的肝脏门管区有少量至中等数量的淋巴细胞、巨噬细胞和嗜酸性粒细胞浸润。同时,门管区胶原增加并延伸至小叶间隔,导致肝实质受压萎缩。作为氧化应激标志物测定的硫代巴比妥酸反应性物质浓度以及氧化型谷胱甘肽与还原型谷胱甘肽的比率显著升高。

结论

氧化改变的存在可能与慢性炎症反应的形态学证据以及细胞肿胀、过氧化物酶体和溶酶体增多所表明的肝细胞损伤有关。