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[酒精对大鼠肝血窦内皮细胞窗孔的影响]

[The influence of alcohol on the liver sinusoids endothelial cell fenestrae of rats].

作者信息

Wang Bing-yuan, Fu Bao-yu, Zhang Jian, Ju Xiao-hua, Cao Yan-xue

机构信息

Department of Gastroenterology, The First Affiliated Hospital of China Medical University, Shenyang 110001, China.

出版信息

Zhonghua Gan Zang Bing Za Zhi. 2004 Aug;12(8):479-81.

Abstract

OBJECTIVE

To study the influence of alcohol on the liver sinusoids endothelial cell (LSEC) fenestrae of rats.

METHODS

Setting up the rat model of alcoholic liver disease by orogastric administration of alcohol, then kill the experimental and control groups of rats at the end of 4 weeks, 8 weeks and 12 weeks after alcohol feeding, and also at the end of another 12 weeks after balance foods feeding succeeding with alcohol feeding for 12 weeks. Staining the liver tissue by means of HE method and observing the successive change of LSEC fenestrae by transmission electron microscope.

RESULTS

The normal LSEC was flat with nucleus and organelle arranged regularly. The distal cytoplasm displayed as lamina with many fenestrae, not accompanied by basement membrane (BM) formation under the endothelial cell. At the end of 4 weeks of alcohol feeding, fenestrae decreased at the partial distal LSEC cytoplasm, but no BM developed. At the end of 8 weeks, fenestrae decreased significantly, even disappeared, with the BM developed incompletely under the endothelial cell. Concomitantly, fibroblast with active function developed. At the end of 12 weeks, the changes became more obvious; the complete BM could even be seen. However, this kind of changes was mostly limited in the single or adjoining sinusoids, as well as with little widespread formation of fibrosis. At the end of 12 weeks of stopping alcohol feeding, defenestrae and development of BM attenuated obviously.

CONCLUSION

The defenestrae and BM of LSEC develop gradually with the chronic alcohol stimulation. Sinusoid capillarization and liver fibrosis even form when significant changes happen. The early change of the limited defenestrae and capillarization may be the basis of alcohol periportal fibrosis formation. This kind of liver fibrosis can be reversible after stopping alcohol feeding.

摘要

目的

研究酒精对大鼠肝血窦内皮细胞(LSEC)窗孔的影响。

方法

通过灌胃给予酒精建立酒精性肝病大鼠模型,于酒精喂养4周、8周、12周结束时,以及在酒精喂养12周后给予平衡饲料喂养12周结束时,处死实验组和对照组大鼠。采用苏木精-伊红(HE)法对肝组织进行染色,并通过透射电子显微镜观察LSEC窗孔的连续变化。

结果

正常LSEC扁平,细胞核和细胞器排列规则。远端细胞质呈板层状,有许多窗孔,内皮细胞下无基底膜(BM)形成。酒精喂养4周结束时,部分远端LSEC细胞质窗孔减少,但无BM形成。8周结束时,窗孔明显减少甚至消失,内皮细胞下BM发育不完全。同时,出现具有活跃功能的成纤维细胞。12周结束时,变化更加明显;甚至可见完整的BM。然而,这种变化大多局限于单个或相邻的血窦,且很少有广泛的纤维化形成。停止酒精喂养12周结束时,窗孔缺失和BM发育明显减轻。

结论

LSEC的窗孔缺失和BM随着慢性酒精刺激而逐渐发展。当发生显著变化时,甚至会形成血窦毛细血管化和肝纤维化。有限的窗孔缺失和毛细血管化的早期变化可能是酒精性门周纤维化形成的基础。这种肝纤维化在停止酒精喂养后是可逆的。

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