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目的 探讨前列环素I2 (PGI2 )和胰高糖素 (GG)在大鼠肝纤维化发病中的作用及肝纤维化形成过程中白介素 (IL 10 )对二者的影响。方法 选取SD大鼠 81只 ,随机分为 3组。对照组 2 1只 (N组 ) ;肝纤维化组 30只 (C组 ) ;干预组 30只 (E组 )。于第5 ,7和 9周分别随机选取C组、E组动物各 10只 ,N组动物 7只 ,颈总动脉插管取血分离血浆 ,后留取肝脏 ,HE染色。采用放射免疫分析方法检测血浆 6 酮 前列腺素F1α( 6 K PGF1α)和GG水平。结果 C组血浆 6 K PGF1α和GG水平显著高于N组和E组 ,经IL 10干预后 ,二者水平下降 ,与N组差异无显著性。在肝纤维化形成过程中 ,大鼠血浆 6 K PGF1α及GG水平呈逐渐上升趋势。结论 前列环素和胰高糖素参与CCL4诱导大鼠肝纤维化形成过程 ,白介素 10对二者有拮抗作用
Objective To investigate the effects of PGI2 and glucagon (GG) on the pathogenesis of hepatic fibrosis in rats and the effects of interleukin (IL 10) on them during the formation of hepatic fibrosis. Methods Totally 81 SD rats were randomly divided into three groups. Control group, 21 (N group); liver fibrosis group 30 (C group); intervention group 30 (E group). Group C, 10 animals in group E and 7 animals in group N were randomly selected at weeks 5, 7 and 9, respectively. Blood was collected from the common carotid arteries to separate the plasma, and the liver was harvested for HE staining. Radioimmunoassay was used to detect plasma 6-ketoprostaglandin F1α (6 K PGF1α) and GG levels. Results The levels of plasma 6 K PGF1α and GG in group C were significantly higher than those in groups N and E. However, the levels of 6 K PGF1α and GG in group C were significantly decreased after intervention with IL 10. During the process of hepatic fibrosis, the levels of 6 K PGF1α and GG in plasma of rats gradually increased. Conclusions Both prostacyclin and glucagon are involved in the process of hepatic fibrosis induced by CCL4, and interleukin 10 antagonizes both of them