Influence of heme oxygenase-1 expression on immune liver fibrosis induced by cobalt protoporphyrin in rats

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.TypeⅠandⅢcollagens 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.

Ursodeoxycholic acid treatment improves hepatocyte ultrastructure in rat liver fibrosis

AIM: To examine the ultrastructural changes after ursodeoxycholic acid (UDCA) treatment in hepatocytes from experimentally induced fibrotic livers.METHODS: Liver fibrosis was induced in male Sprague-Dawley rats with CCl4 for 12 wk, and the rats were divided into two groups. Group I was treated with saline and group Ⅱ with UDCA (25 mg/kg per day) for 4 wk. All the rats were killed at wk 16. Mitochondria, nuclei, rough endoplasmic reticulum (RER) and smooth endoplasmic reticulum (SER) of hepatocytes were evaluated according to a scoring system.RESULTS: Mitochondria, nuclei, RER and SER injury scores in group Ⅱ were significantly lower than those in groupⅠ(P < 0.001). CONCLUSION: UDCA alleviates hepatocyte organelle injury in CCl4-induced liver fibrosis.