Reactive oxygen intermediates and eicosanoid production by Kupffer cells and infiltrated macrophages in acute and chronic liver injury induced in rats by CCl4
Reactive oxygen intermediates and eicosanoid production by Kupffer cells and infiltrated macrophages in acute and chronic liver injury induced in rats by CCl4
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DOI：
10.1007/s000110050649
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发表时间：
2000-12-01
影响因子：
6.7
通讯作者：
Vinel, JP
中科院分区：
文献类型：
--
作者：
Alric, L;Orfila, C;Vinel, JP
目标与设计：本研究的目的是表征在急性和慢性肝损伤引起的四氯化碳，巨噬细胞表型和是否在活性氧中间体（ROI）和类花生酸生产的枯否细胞（KC）的变化observed.Material和方法：肝脂肪坏死和肝硬化大鼠诱导后3周和9周的四氯化碳中毒，分别。使用单克隆抗体艾德-1通过免疫组织化学研究鉴定单核细胞和组织巨噬细胞，使用抗体艾德-2鉴定组织巨噬细胞。释放的ROI和类花生酸响应佛波醇酯TPA（蛋白激酶激活剂）和钙离子载体A23187在培养cells.Results：与健康对照组相比，脂肪坏死或肝硬化大鼠的肝脏表现出显着增加的艾德-1和艾德-2阳性细胞。发现只有来自肝脂肪坏死大鼠的KC具有比健康对照更高的A23187、TPA + A23187或调理酵母多糖诱导的ROI产生（p < 0.01）。TPA + A23187或调理酵母多糖刺激后，与健康对照组相比，脂肪坏死或肝硬化大鼠KC产生更多的TxB 2和白三烯，而PGE 2减少（p
Objective and Design: The aim of the present study was to characterize during acute and chronic liver injury induced by CCl4, macrophage phenotypes and whether a change in reactive oxygen intermediates (ROI) and eicosanoids production by Kupffer cells (KC) was observed.Material and Methods: Liver steato-necrosis and cirrhosis were induced in rats after 3 weeks and 9 weeks of CCl4 intoxication, respectively. Monocytes and tissue macrophages were identified by immunohistochemical study using monoclonal antibodies ED-1 and tissue macrophages using the antibody ED-2. The release of ROI and eicosanoids in response to the phorbol ester TPA (protein kinase activator) and to the calcium ionophore A23187 was assessed in cultivated cells.Results: As compared to healthy controls, livers of rats with steato-necrosis or cirrhosis exhibited a significant increase of ED-1 and ED-2 positive cells. Only KC from rats with liver steato-necrosis were found to have higher A23187, TPA + A23187 or opsonized zymosan induced ROI production than healthy controls (p < 0.01). After TPA + A23187 or opsonized zymosan stimulation, KC from both rats with steato-necrosis or cirrhosis produced more TxB2 and leukotrienes and less PGE2 as compared to healthy controls (p