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
DUAN Zhi-jun YANG Dong WANG Fei SUN Ying-jie SUN Xiao-yu ZHENG Miao-lei
