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慢性肝炎肝细胞线粒体超微结构改变及与凋亡蛋白的关系 被引量:1

Correlation between mitochondria ultramicrostructure alteration and apoptotic protein of liver cells in chronic hepatitis
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摘要 目的 为研究慢性肝炎时肝细胞凋亡的途径及线粒体在凋亡过程中所起的作用。方法 对72例慢性肝炎及29例肝炎后肝硬化的活检肝组织进行了各种凋亡蛋白的免疫组化观察;并对其中15例慢性肝炎患者肝细胞凋亡时线粒体的改变进行了超微结构观察。结果肝细胞中促凋亡蛋白(Fas、FasL、Bax)在肝炎组表达明显高于肝硬化组(P<0.001),但抑凋亡蛋白(Bcl—2、Bcl-XL、Bcl-2α)在肝硬化组的表达强于慢性炎组。对15例慢性肝炎(按肝组织学分类轻度10例、中度1例、重度1例,肝硬化3例)的364个肝细胞超微结构观察,发现40个(11.0%)肝细胞线粒体具有多种损伤,包括线粒体的外膜破裂及内膜和外膜之间的基质溢出于肝细胞胞浆中的现象均清晰可见结论慢性肝炎时有多数线粒体受到损害,线粒体外膜破裂,基质外溢于肝细胞浆,支持近年对凋亡研究的观点,即肝细胞凋亡主要属于内源性凋亡(或称Ⅱ型凋亡)。 Objective It is to study the pathway of apoptosis occurred in chronic hepatitis and the role of mitochondria in the process of programmed cell death. Methods Liver biopsy specimens from 72 cases of chronic hepatitis and 29 cases of post hepatitic cirrhosis were studied immunohistochemically. Specimens of 15 cases of chronic hepatitis were examined for the ultramicrostructure of their mitochondria abnormality. Results The expression of proapoptotic protein (Fas, FasL, Bax) in the hepatocytes was found significantly higher in chronic hepatitis group than that in cirrhosis group(P < 0.001) ,In the ultramicrostructure examination of the 15 cases of chronic hepatitis (including 10 cases of mild, 3 cases of moderate and 2 cases of severe histologically) , 364 hepatocytes were examined, out of which 40 (11.0% ) hepatocytes were found with various kinds of destruction in their mitochondria. The rupture of the outer membrane of mitochondria and the leakge of matrix from the in-termembrane space were definitely demonstrated. Conclusion The numerous damaged mitochondria with ruptured outer membrane found in chronic hepatitis may serve as a direct support for the recent viewpoint that apoptosis of liver cells principally proceeds through the intrinsic pathway or type Ⅱapoptosis.
出处 《胃肠病学和肝病学杂志》 CAS 2004年第3期283-286,共4页 Chinese Journal of Gastroenterology and Hepatology
基金 国家自然科学基金(NO.39770660) 北京军区重点课题(NO.95B008) 连云港市社会发展项目(SH0210)
关键词 慢性肝炎 肝细胞 线粒体 超微结构 凋亡蛋白 免疫组化 Chronic hepatitis Hepatocellular Apoptosis protein Mitochondria Ultramicrostructure
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