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目的 研究病毒性肝炎肝细胞凋亡及与肝纤维化的关系。方法 以原位末端标记及免疫组化检测 40例慢性病毒性肝炎 (CH)肝组织细胞凋亡相关线状断裂DNA以及Fas抗原、转化生长因子 β1(TGF β1)、Ⅲ型前胶原肽 (PⅢP)在肝组织中的表达 ;以酶联免疫吸附测定 (ELISA)检测血清可溶性Fas(sFas)及TGF β1。 结果 CH肝细胞DNA损伤与肝组织Fas抗原、TGF β1表达及血清sFas、TGF β1水平明显相关 (r =0 6 2 19,0 5 36 8,0 5 5 6 4,0 5 996。P <0 0 5～ 0 0 1) ;重度CH及肝硬变患者DNA损伤程度明显高于轻度CH患者 ,且与肝组织PⅢP、TGF - β1的表达明显相关。结论 sFas可能也是促进肝细胞凋亡的因素之一。在肝细胞凋亡的同时伴有胶原等细胞外基质合成的增加 ,而TGF β1在细胞凋亡与肝纤维化之间可能起着极为重要的桥梁作用。
Objective To study the relationship between hepatocellular apoptosis and hepatic fibrosis in viral hepatitis. Methods 40 cases of chronic hepatitis B (CH) hepatocellular apoptosis-associated linear cleavage DNA, Fas antigen, transforming growth factor β1 (TGFβ1), procollagen Ⅲ (PⅢP) In liver tissue. Serum soluble Fas (sFas) and TGF-β1 were detected by enzyme linked immunosorbent assay (ELISA). Results DNA damage of CH hepatocytes was significantly associated with the expression of Fas antigen, TGFβ1 and the levels of sFas and TGFβ1 in liver tissue (r = 0 6 2 19,0 5 36 8,0 5 5 6 4,0 5 996.P <0 0 5 ~ 0 0 1). The DNA damage in patients with severe CH and cirrhosis was significantly higher than that in patients with mild CH, and the expression of PⅢP and TGF - β1 was significantly correlated with liver tissue. Conclusion sFas may also be one of the factors that promote hepatocyte apoptosis. In hepatocyte apoptosis accompanied by an increase in extracellular matrix synthesis of collagen, TGFβ1 may play an important bridging role between apoptosis and hepatic fibrosis.