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AIM:To investigate the potential protective effect of HO-1 on cirrhotic liver cells in rats. METHODS:Male Wistar rats included in the current study were randomly divided into 5 groups as follows: normal(N)group;liver cirrhotic(LC)group;sham(S) group;I/R group and I/R+heroin group.The model for inducing liver cirrhosis in rats was established according to a previously published protocol.Following this the segmental hepatic ischemia reperfusion operation was carried out.The rats were treated with 30μmol/kg hemin(HO-1 inducer,ferric portoporphyrin IX chloride) i.p.or 0.9% NaCl(control)24 h and 12 h before hepatic ischemia for 30 min or sham laparotomy.Blood was collected for serum enzymatic measurement 6 and 12 h after reperfusion or sham laparotomy.HO-1, NF-_KB and caspase-3 expressions were assessed by immunohistochemical analysis. RESULTS:The expressions of proteins are inversely correlated to the gray values.HO-1 expression in the I/R+hemin group was increased significantly than I/R group at 6 h and 12 h after hepatic I/R(6 h:112.0±8.3 vs 125.1±5.7,P<0.01;12 h:120.8±11.0 vs 132.4±6.2,P<0.01).Hemin improved serum manganese superoxide dismutase(MnSOD)(6 h:131.3±17.6 vs 107.0±13.9,P<0.01;12 h:141.4±12.5 vs 118.3±10.2,P<0.01),lessened liver cell injury,decreased caspase-3(6 h:166.7±8.1 vs 145.5±14.6,P<0.01; 12 h:172.8±3.8 vs 148.0±6.5,P<0.01)and NF-_kB expression(6 h:150.2±8.6 vs 139.7±6.0,P<0.01; 12 h:151.1±5.9 vs 148.1±5.3,P>0.05)and serum alanine aminotransferase(ALT)(6 h:413.3±104.1 vs 626.8±208.2,P<0.01;12 h:322.2±98.8 vs 425.8±115.4,P<0.05),aspartate aminotransferase(AST)(6 h: 665.2±70.1 vs 864.3±70.4,P<0.01;12 h:531.1±98.6 vs 664.4±115.6,P<0.01),malondialdehyde (MDA)levels(6 h:11.1±2.17 vs 13.5±2.01,P<0.01; 12 h:9.36±1.10 vs 10.8±1.62,P<0.05)in the I/R+ hemin group when compared with the I/R group. CONCLUSION:These results suggest that HO-1 plays an important role in protecting liver cells from hepatic I/R injury in cirrhotic rats by decreasing oxidative stress, apoptosis and inflammation.
AIM: To investigate the potential protective effect of HO-1 on cirrhotic liver cells in rats. METHODS: Male Wistar rats included in the current study were divided divided into 5 groups as follows: normal (N) group; liver cirrhotic (LC) group ; sham (S) group; I / R group and I / R + heroin group. The model for inducing liver cirrhosis in rats was established according to a previously published protocol. Focusing on the segmental hepatic ischemia reperfusion operation was carried out. The rats were treated with 30 μmol / kg hemin (HO-1 inducer, ferric portoporphyrin IX chloride) ipor 0.9% NaCl (control) for 24 h and 12 h before hepatic ischemia for 30 min or sham laparotomy. Blood was collected for serum enzymatic measurement 6 and RESULTS: The expressions of proteins are inversely correlated to the gray values. HO-1 expression in the I / R + 12 h after reperfusion or sham laparotomy. HO-1, NF-κB and caspase- hemin group was increased significantly than I / R group at 6 h and 12 h after hepatic I / R (6 h: 112.0 ± 8.3 vs 125.1 ± 5.7, P <0.01; 12 h: 120.8 ± 11.0 vs 132.4 ± 6.2, P <0.01) .Hemin improved serum manganese superoxide dismutase (6 h: 131.3 ± 17.6 vs 107.0 ± 13.9, P <0.01; 12 h: 141.4 ± 12.5 vs 118.3 ± 10.2, P <0.01) and lessened liver cell injury 8.1 vs 145.5 ± 14.6, P <0.01; 12 h: 172.8 ± 3.8 vs 148.0 ± 6.5, P <0.01) and NF-κB expression (6 h: 150.2 ± 8.6 vs 139.7 ± 6.0, P <0.01; ± 5.9 vs 148.1 ± 5.3, P> 0.05) and serum alanine aminotransferase (ALT) (6 h: 413.3 ± 104.1 vs 626.8 ± 208.2, P <0.01; 12 h: 322.2 ± 98.8 vs 425.8 ± 115.4, P < (6 h: 665.2 ± 70.1 vs 864.3 ± 70.4, P <0.01; 12 h: 531.1 ± 98.6 vs 664.4 ± 115.6, P <0.01) and malondialdehyde 13.5 ± 2.01, P <0.01; 12 h: 9.36 ± 1.10 vs 10.8 ± 1.62, P <0.05) in the I / R + hemin group when compared with the I / R group. CONCLUSION: These results suggest that HO-1 plays an important role in protecting liver cells from hepatic I / R injury in cirrhotic rats by decreasing oxidative stress,apoptosis and inflammation.