背景 Heme oxygenase (惊讶) 在一些肝疾病起作用,但是它在有免疫力的肝纤维变性做的,是很少报导了。我们在老鼠免疫者肝纤维变性调查了 HO-1 的规定机制发现为 intervention.Methods 男性 Sprague-Dawley 老鼠的线路随机被划分成控制组( N , n=12 ),纤维变性组( F , n=20 ),劝诱组的钴 protoporphyrin ( CoPP )(公司, n=20 )并且禁止组的锌 protoporphyrin ( ZnPP )( Zn , n=20 )。在组 F,公司和 Zn,有免疫力的肝纤维变性与人的浆液白朊被建立。在攻击阶段, CoPP (5mg/kg ) 和 ZnPP (5 mg/kg ) intraperitoneally 分别地在组公司和 Zn 被注射。在老鼠模型的建立以后,老鼠的数字分别地在组 N, F,公司和 Zn 归结为 11, 15, 17 和 12,因为在这个过程期间的死亡。在肝的 HO-1 被弄污的 Westem 和 immunohistochemistry 检测。纤维变性的索引被放射性免疫测定估计。转变生长 factor-1 (TGF-1 ) 的浆液的集中,和 metalloproteinses (TIMP-1 ) 的织物禁止者用连接酶的 immunosorbent 试金被检测。肝的星形的房间(HSC ) 和纤维变性的增长度被病理学的检查估计。数据分析被社会科学统计套装软体 10.0software .Results 执行 HO-1 在的表达式组 F 在组 N 比那显著地高,但是在组公司(P 0.05 ) 比那降低;当那在组 Zn 比在组 F ( P 0.05 )低时,但是比那仍然高在有组 N ,功能的肝和肝的组 N ( P 0.01 ) .Compared ,纤维变性指示物在组 F ( P 0.01 )被增加,当比较组织 F 时,他们在组公司( P 0.05 )被减少并且在组 Zn ( P 0.05 )增加了。CoPP 与组 F (P 0.01 ) 比较减少了 hepatocellular 损害和肝的纤维变性的程度,是 ZnPP (P0.01 ) 的相反的效果。HSC 用间接方法被观察,结果证明在组 F 的 HSC 的数字在组 N 和公司多于那增加了,当时不到在里面组 Zn。当 HO-1 逐渐地表示了时, TGF-1 的集中减少了(组公司:( 3.5 楴敶爠瑡 ? 湡 ? 敫灥琠敨映污敳渠来瑡癩?
Background Heme oxygenase (HO) plays roles in some liver diseases, but what it does in immune liver fibrosis is rarely reported. We investigated the regulation mechanisms of HO-1 in rat immune liver fibrosis to find routes for intervention. Methods Male Sprague-Dawley rats were randomly divided into control group (N, n=-12), fibrosis group (F, n=20), cobalt protoporphyrin (CoPP) inducing group (Co, n=20) and zinc protoporphyrin (ZnPP) inhibiting group (Zn, n=20). In groups F, Co and Zn, immune liver fibrosis was established with human serum albumin. At the attacked stage, CoPP (5 mg/kg) and ZnPP (5 mg/kg) were intraperitoneally injected in groups Co and Zn, respectively. After establishment of rat models, the numbers of rats reduced to 11, 15, 17 and 12 in groups N, F, Co and Zn respectively, because of death during the process. HO-1 in liver was detected by Western blotting and immunohistochemistry. The indexes of fibrosis were assessed by radioimmunoassay. Concentrations of serum transforming growth factor-β1 (TGF-β1), and tissue inhibitor of metalloproteinses (TIMP-1) were detected using enzyme-linked immunosorbent assay. Hepatic stellate cell (HSC) and proliferation degree of fibrosis were assessed by pathological examination. Data analysis was performed by SPSS 10.0 software. Results The expression of HO-1 in group F was significantly higher than that in group N, but lower than that in group Co (P 〈0.05); while that in group Zn was lower than in group F (P 〈0.05), but still higher than that in group N (P 〈0.01). Compared with group N, liver functional and liver fibrosis indicators were increased in group F (P 〈0.01), while comparing to group F, they were decreased in group Co (P 〈0.05) and increased in group Zn (P 〈0.05). CoPP reduced the extent of hepatocellular injury and hepatic fibrosis in comparison with group F (P 〈0.01), being the opposite effect of ZnPP (P 〈0.01). HSC was observed using indirect method a