前列腺素E_1对日本血吸虫病大鼠肝纤维化形成的影响

THE EFFECT OF PROSTAGLANDIN E_1 ON HEPATIC FIBROGENESIS IN RATS WITH SCHISTOSOMIASIS JAPONICA

目的 探讨前列腺素 E1 (PGE1 )对日本血吸虫病肝纤维化形成的影响及其机制。 方法 用免疫组化 SABC技术结合计算机彩色病理图文分析系统 ,定量检测并分析 PGE1 治疗前后 ,感染日本血吸虫大鼠肝内 、 型胶原及转化生长因子 β1 (TGF- β1 )的变化。 结果 (1)感染组大鼠肝内 、 型胶原及 TGF- β1 均主要分布在虫卵肉芽肿内 ,呈密集片状着色。经 PGE1 治疗后 、 型胶原及 TGF- β1 的着色均明显减少。 (2 ) PGE1 治疗组 、 型胶原及 TGF- β1 的含量分别为 0 .2 5 71Sv± 0 .1939、0 .2 45 9Sv± 0 .1836和 0 .135 1Sv± 0 .0 941(Sv为面密度 )均显著低于感染对照组的 0 .475 9Sv± 0 .2 40 1、0 .46 12 Sv± 0 .1987和 0 .34 5 0 Sv± 0 .2 15 2 (P<0 .0 5 ) ;(3)在 PGE1 治疗组和感染对照组大鼠肝内 , 型胶原的含量均与 TGF- β1 的含量呈显著正相关 (r=0 .96 36 ,P<0 .0 5 ;r=0 .86 6 7,P<0 .0 5 ) , 型胶原的含量亦均与 TGF- β1 的含量呈显著正相关 (r=0 .96 36 ,P<0 .0 5 ;r=0 .92 72 ,P<0 .0 5 )。 结论 PGE1 对日本血吸虫病肝纤维化的形成有抑制作用 ,其机理可能与 PGE1 抑制 TGF- β1 的表达有关。

Objective To investigate the effect of prostaglandin E 1 (PGE 1) on hepatic fibrogenesis and its mechanism in rats with schistosomiasis japonica. Methods The changes of type Ⅰ collagen, type Ⅲ collagen and transforming growth factor beta 1 (TGF-β 1) in the livers were determined by immunohistochemical streptavidin biotin-peroxidase complex method and computer multimedia pathologic picture analysis before and after rats with schistosomiasis japonica were treated by PGE 1. Results (a) Type Ⅰ collagen, type Ⅲ collagen and TGF-β 1 were mainly distributed in egg granulomas in the liver of infected rats, which showed dense coloration and became thin coloration after PGE 1 treatment. (b) Amounts of typeⅠ collagen, type Ⅲ collagen and TGF-β 1 were 0.2571±0.1939, 0.2459±0.1836 and 0.1351±0.0941 respectively in PGE 1 treated-group, which were less than those (0.4759±0.2401, 0.4612± 0.1987 and 0.3450±0.2152 respectively) of control-group(P<0.05). (c) In infected rats with or without PGE 1 treatment, a positive correlation could be demonstrated by Spearman analysis between type Ⅰ collagen and TGF-β 1(r=0.9636,P<0.05;r=0.8667,P< 0.05 respectively); and that between type Ⅲ collagen and TGF-β 1(r=0.9636,P<0.05,r=0.9272,P<0.05, respectively). Conclusion PGE 1 significantly suppressed hepatic fibrogenesis in schistosomiasis japonica, whose mechanism was probably associated with suppressing of TGF-β 1 expression by PGE 1.