摘要
目的：研究Ｆａｓ和Ｆａｓ配体（ＦａｓＬ）在乙型肝炎肝细胞凋亡及坏死中的作用。方法：分别用免疫组织化学方法和原位末端标记技术（ＴＵＮＥＬ试验）检测７１例各种类型乙型肝炎患者肝组织Ｆａｓ／ＦａｓＬ表达和肝细胞凋亡情况。结果：１．ＴＵＮＥＬ试验中度以上阳性，慢性迁延性肝炎（ＣＰＨ）为３１．６％（６／１９）、慢性活动性肝炎（ＣＡＨ）为１００％（２４／２４）、肝硬化（ＬＣ）为２２．２％（２／９）、重型肝炎（ＦＨ）为７８．９％（１５／１９）。２．Ｆａｓ表达中度以上阳性，ＣＰＨ为３６．８％（７／１９）、ＣＡＨ为９１．７％（２２／２４）、ＬＣ为５５．６％（５／９）、ＦＨ为７３．７％（１４／１９）。３．ＦａｓＬ表达中度以上阳性，ＣＰＨ为２１．１％（４／１９）、ＣＡＨ为７９．１％（１９／２４）、ＬＣ为５５．６％（５／９）、ＦＨ为９４．７％（１８／１９）。肝细胞凋亡及Ｆａｓ和ＦａｓＬ表达的阳性程度，在各型乙型肝炎中的分布均有显著性差异（Ｐ值＜０．００５）。部分病例肝细胞同时有Ｆａｓ和ＦａｓＬ表达。结论：Ｆａｓ和ＦａｓＬ在肝细胞凋亡和坏死中起重要作用，肝细胞的直接自杀方式或自分泌及旁分泌杀伤机制，可能为乙型病毒性肝炎发病机理的重要?
Aim: To evaluate the role of Fas acttigen (FasAg) and Fas ligand (FasL) on hepatic apoptosis and necrosis ln viral hepatitis B. Methods: Paraffin sections (n=71 ) from patients with HBV infection (M: F 57: 14, age 20-79, CPH19, CAH24, cirrhods 9, fulminant hepatitais 19) were studied. 5 casa of atormal Uver tissues were studied as control. Apoptosis was detected by terminal deoxynucleotidyl transferase (TdT) mediated dUTP nick end labeling (TUNEL) . FaAg and FasL were determdned by immunohistochemistry. Results: Hepatic apoptosis and the expression of FasAg/FasL on hepatocytes were not detected in nonmal liver tissues. ln contrast to it, there were a strong reaction in TUNEL assay and FasAg/FasL expressed on hepatocytes in liver tissues infected with HBV. Our oborations also showed that FasAg and FasL were mainly detected in cytoplasm, and the degree of apoptosis and the expresdon of FasAg/FasL on hepatocytes had distinct difference in different hepatitis (P<0.005). There was a positive correlation between degree of the expression of FasAg/FasL on hepatocytes and hepatic apoptods(P<0.005). It was significantly that some hepatocytes expressed both FasAg and FasL, and many FasAg and/or FasL positive cells did not accompany with liver infiltrating lymphocytes. Conclusion: HBV perhaps induca expression of FasAg and FasL on hepatocytes. The interaction of FasAg and FasL on hepatocytes might result in liver damage, and death of hepatocytes probably occurs by autocrine or paracrine and fratricide mechanisms mediated by the hepatocytes themselves in viral hepatitis B .
出处
《中华肝脏病杂志》
CAS
CSCD
1997年第2期88-90,共3页
Chinese Journal of Hepatology
基金
国家自然科学基金
卫生部及四川省卫生厅科学基金
