丁型肝炎患者肝组织中Bcl-2、Bax和肝细胞凋亡表达

目的 探讨bcl-2、bax及肝细胞凋亡在丁型肝炎发病机理中的作用。方法 采用免疫组织化学单、双标记染色和TUNEL技术、检测77例丁型肝炎患者肝组织HDAg、bcl-1、bax及肝细胞凋亡表达，以67例乙型肝炎作对照，结果 bcl-2和bax均以肝细胞浆表达为主。HDAg以肝细胞核表达为主。HDAg和Bax与凋亡细胞表达及分布有相关性，三成分在各型肝炎中的表达强度差异有显著意义（P＜0.05）。结论 HDAg、bax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，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。

Expression of bcl-2, bax and hepatocyte apoptosis in the liver tissues of hepatitis D patients

Objective: To study the role of bcl-2, bax and hepatocyte apoptosis in the pathogenesis of hepatitis D. Methods Expression of HDAg, bcl-2, bax, and hepatocyte apoptosis in liver specimens of 77 patients with hepatitis D were studied by immunohistochemistry, double labelling and serial sections, and TUNEL assay. Six-seven hepatitis B patients served as control. Results Bcl-2 and bax were mainly expressed in the cytoplasm of hepatocytes, and HDAg mainly in the nucleus of hepatocytes. A large number of HDAg and bax positive cells were distributed among infiltrating lymphocytes at the periportal region in which many apoptosis hepatocytes were found. There were positive correlations between the expression of bax, HDAg and hepatocyte apoptosis (P<0.05). Conclusions The distribution and the expression of bax, HDAg and hepatocyte apoptosis are significantly correlated with the activity of inflammation and the seventy of the liver damage. Hepatitis D virus infection may induce the expression of bax in the hepatocytes and exacerbate hepatocyte apoptosis through which take a part in the pathogenesis of hepatitis D.