血红素加氧酶-1表达对钴原卟啉诱导的大鼠免疫性肝纤维化的影响。
Influence of heme oxygenase-1 expression on immune liver fibrosis induced by cobalt protoporphyrin in rats.
作者信息
Wang Fei, Duan Zhi-Jun, Sun Ying-Jie
机构信息
Department of Gastroenterology, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China.
出版信息
World J Gastroenterol. 2009 Jun 28;15(24):3009-14. doi: 10.3748/wjg.15.3009.
AIM
To investigate the effect of heme oxygenase-1 (HO-1) expression on immune liver fibrosis induced by cobalt protoporphyrin (CoPP) in rats.
METHODS
An immune liver fibrosis model of rat was established by administering human serum albumin (HSA). The rats were divided into CoPP, liver fibrosis and normal control groups. Rats in the CoPP group received intraperitoneal CoPP concurrently with HSA. Expression of HO-1 protein was observed by Western blotting and immunohistochemistry. Hematoxylin and eosin (HE) staining was performed to assess fibrosis proliferation and distribution, proliferation extent of fibroblasts, and alterations in hepatocytes and inflammatory cells. Type I and III collagens were detected with Van Gieson's (VG) staining and Foot's reticular fiber staining, respectively. In addition, spindle-shaped cells existing at perisinusoidal locations beyond portal and septa areas were investigated with HE staining.
RESULTS
Western blotting and immunohistochemistry showed that the expression of HO-1 protein was higher in the CoPP group than in the liver fibrosis group (P < 0.05). Compared with the liver fibrosis group, the serological index of hepatic fibrosis in the CoPP group decreased significantly (P < 0.05). HE, VG and Foot's staining revealed that administration of CoPP reduced the extent of hepatic fibrosis. The levels of serological indicators and the number of spindle-shaped cells at perisinuous locations beyond the portal and septa areas were reduced in the CoPP group. Only a few inflammatory cells were seen around the portal areas and central veins in the CoPP group.
CONCLUSION
Increased endogenous HO-1 may suppress liver fibrosis by protecting liver cells, inhibiting inflammatory cell infiltration and hepatic stellate cell transformation.
目的
探讨血红素加氧酶-1（HO-1）表达对钴原卟啉（CoPP）诱导的大鼠免疫性肝纤维化的影响。
方法
通过给予人血清白蛋白（HSA）建立大鼠免疫性肝纤维化模型。将大鼠分为CoPP组、肝纤维化组和正常对照组。CoPP组大鼠在给予HSA的同时腹腔注射CoPP。采用蛋白质印迹法和免疫组织化学法观察HO-1蛋白的表达。进行苏木精-伊红（HE）染色以评估纤维化的增殖和分布、成纤维细胞的增殖程度以及肝细胞和炎性细胞的变化。分别用Van Gieson（VG）染色和Foot网状纤维染色检测Ⅰ型和Ⅲ型胶原。此外，用HE染色研究门静脉和间隔区域以外的肝血窦周围存在的梭形细胞。
结果
蛋白质印迹法和免疫组织化学法显示，CoPP组HO-1蛋白的表达高于肝纤维化组（P<0.05）。与肝纤维化组相比，CoPP组肝纤维化的血清学指标显著降低（P<0.05）。HE、VG和Foot染色显示，给予CoPP可减轻肝纤维化程度。CoPP组血清学指标水平以及门静脉和间隔区域以外的肝血窦周围梭形细胞数量减少。CoPP组门静脉区和中央静脉周围仅见少量炎性细胞。
结论
内源性HO-1增加可能通过保护肝细胞、抑制炎性细胞浸润和肝星状细胞转化来抑制肝纤维化。
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