Skolosidal Ajanlardan Kaynaklanan Sklerozan Kolanjitin Önlenmesinde Halofuginon ve Ursodeoksikolik Asidin Etkileri

Abstract

Aim: Biliary sclerosis is a life treatening condition caused by auto-immunity, operative trauma, toxic agents, cancer and chronic inflammatory conditions. The liver tissue may progress into overt cirrhosis by the progression of fibrotic scar tissue. Halofuginone, which is the active component of the plant alkaloid febrifugine, has been shown to inhibit fibrosis. Material and Method: Fifty rats were randomized on 5 groups to form a biliary sclerosis model by a scolocidal agent povidone iodine(PI) injection into the common bile duct with a control group of saline infusion included. The four PI groups were later treated by halofuginone, ursodeoxycholic acid (UDCA), with both and none. The rats were sacrificed 90 days later for intrahepatic and hilar fibrosis. Laboratory parameters of liver damage and levels of hydroxypryroline to show collagen degradation were obtained and histological examination of the liver and the common bile duct for fibrotic changes were carried out. Results: With or without application of ursodeoxycholic acid, the halofuginone groups showed significantly less sclerosis according to histological analysis. In regard to serum analysis of SGOT, SGPT and ALP; there were significant differences between “PI only” group and halofuginone groups. GGT was significantly high in “PI only” group. There was not any significant difference between the groups in regard to bilirubin levels. Hydroxyproline serum levels were highest in “PI only” group, followed by “UDCA only” group and then halofuginone groups.Conclusion: Halofuginone was effective in preventing fibrosis as an additional medical therapy to UDCA in an induced sclerosing cholangitis model in rats.