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Bcl-2/bax、Bak介导的肝细胞凋亡在丁型肝炎病情重型化机制中的作用
Role of Bcl-2/Bax in hepatocyte apoptosis in tissues of hepatitis D.
【摘要】 目的 探讨Bcl 2 /bax、Bak及其介导的肝细胞凋亡在病情重型化机制中的作用。方法 采用刊TUNEL技术和免疫组化单、双标记染色 ,检测 77例丁肝病人肝组织中HDAg、bcl 2、bax和Bak表达及肝细胞凋亡情况。以HDV阴性的 67例乙型肝炎作对照。结果 Bcl 2、bax和Bak均以肝细胞浆表达为主。HDAg以肝细胞核表达为主。HDAg、bax和Bak与肝细胞凋亡表达及分布有相关性 ,四成分在各型肝炎中的表达强度有显著性差别意义 (P <0 .0 5 )。结论 HDAg、bax、Bak和肝细胞凋亡表达强度和阳性细胞分布均与肝组织炎症活动及病理损害程度相关 ,HDV感染可诱导肝细胞表达bax和Bak ,增强肝细胞凋亡 ,这一机制在丁型肝炎发病机理中可能有一定重要作用
【Abstract】 Objective To study the relationship of bcl-2 , Bax, Bak and hepatocyte apoptosis in pathogenesis of hepatitis D. Methods Expression of HDAg, bcl-2,bax,Bak and hepatocyte apoptosis in liver specimens of 77 patients with hepatitis D were studied by immunohistochemistry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) technique. Meanwhile, the relationship between expression of HDAg, bcl-2/Bax and hepatocyte apoptosis were studied by double labelling and serial sections. Results Bcl-2 was mainly expressed in the cytoplasm of hepatocytes, Bax and Bak mainly in the cytoplasm of hepatocytes and partly in the nucleus of hepatocytes, and HDAg mainly in the nucleus of hepatocytes. Much of HDAg and Bax or Bak positive cells were distributed among infiltrating lymophocytes at the periportal region especially at the advancing edges of areas of “piecemeal necrosis". Much of hepatocytes apoptosis was found near to positive cells of HDAg. There were positive correlations between degrees of Bax or Bak expression, HDAg expression and hepatocyte apoptosis (P<0.01,P<0.05).Conclution The distribution and the expression of Bax, HDAg and hepatocyte apoptosis are significantly correlated with the activity of inflammation and the severity of the liver damage.HDV infection may induce the expression of Bax and Bak in the hepatocytes.Apoptosis caused by bcl-2, bax/Bak may play an important role in the liver cell injury by HDV infection.
- 【文献出处】 胃肠病学和肝病学杂志 ,Chinese Journal of Gastroenterology and Hepatology , 编辑部邮箱 ,2004年05期
- 【分类号】R512.6
- 【下载频次】90