论文部分内容阅读
目的 探讨bc1 2、bax、Bak在乙型肝炎病毒和丁型肝炎病毒重叠感染患者病情加重机制中的作用。方法 采用免疫组化单、双标记染色技术 ,检测 77例伴HDV感染的乙型肝炎患者肝组织中HDAg、bcl 2、bax和Bak表达。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与Bax和Bak表达及分布有相关性 ,它们在各型肝炎中的表达强度有显著性差异 (P <0 .0 5 )。结论 HDAg、bax、Bak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 ,这一机制在伴HDV感染的乙型肝炎患者病情加重中可能起一定的作用
Objective To investigate the role of bcl-2, bax and Bak in the pathogenesis of hepatitis B virus and hepatitis D virus over-infection. Methods The expression of HDAg, bcl 2, bax and Bak in liver tissue of 77 hepatitis B patients with HDV infection were detected by immunohistochemical single and double labeling staining. HDV-negative 67 cases of hepatitis B as a control. Results bcl 2, Bax and Bak were mainly expressed in liver cytoplasm. HDAg is mainly expressed in hepatocytes. HDAg was associated with the expression and distribution of Bax and Bak, and the expression intensity of HDAg in each type of hepatitis was significantly different (P <0.05). Conclusion The expression of HDAg, bax, Bak and the distribution of positive cells are related to the degree of inflammatory activity and pathological damage in liver tissue. HDV infection can induce the expression of bax and Bak in hepatocytes and enhance the apoptosis of hepatocytes. Hepatitis patients may play a role in exacerbations