复方鳖甲软肝片抗肝纤维化机制的临床病理研究

Clinical pathological study on the mechanism of effect of Fufangbiejiaruanganpian in treatment of liver fibrosis

目的 探讨复方鳖甲软肝片 (FFBJRGP)抗人体肝纤维化的作用机制。方法 6 5例慢性乙型肝炎患者经FFBJRGP治疗前、后(治疗 6个月 )肝穿组织 ,采用Ishak评分系统进行组织学疗效评价。应用原位末端标记技术 (TUNEL)POD法和α SMA单抗免疫组织化学染色法双标记显示肝组织内活化肝星状细胞(HSC)的凋亡状况。结果 与治疗前穿刺肝组织比较 ,FFBJRGP治疗后肝组织炎症活动度和肝纤维化程度均有明显改善 (均P <0 0 1) ,肝组织内活化HSC数量明显减少 ,而凋亡的活化HSC数量则显著增加 (均P <0 0 1)。结论 抑制HSC活化、促进活化HSC凋亡可能为FFBJRGP抗肝纤维化的作用机制之一 ;

Objective To explore the mechanism of Fufangbiejiaruanganpian(FFBJRGP) treating liver fibrosis. Methods Needle biopsies before and after treatment with FFBJRGP were done in 65 patients with chronic viral hepatitis B, and the liver tissues were studied with Ishak scoring system to evaluate the effects of treatment. The activation, proliferation and apoptosis of hepatic stellate cells (HSCs) in the liver specimens were determined by using the double immunohistochemical staining of in situ terminal deoxynucleotidyl transferase mediated dUTP nick end labelling method (TUNEL) and smooth muscle actin (SMA). Results Compared with the specimens before treatment, the stages of liver fibrosis and histological activity grades in liver tissues were significantly improved after treatment with FFBJRGP for 6 months (mean value: P<0.01 respectively). Furthermore, the number of activated HSCs was decreased remarkably after therapy with FFBJRGP, while the apoptosis of activated HSCs was significantly increased (both P<0.01, vs before treatment, respectively). Conclusion Inhibition of activation of HSC and promotion of apoptosis of the activated HSCs might constitute the mechanism of therapeutic effect of FFBJRGP in the prevention of fibrosis of the liver.