The Effect of Ursodeoxycholic Acid on Messenger RNA Hepcidin Expression Associated with Liver Fibrosis in Perposed Cholestasis Jaundice

Molecular pathways associated with chronic inflammation of the liver that causes fibrosis of the liver was investigated further. Current treatment is to focus on the etiology and to eliminate oxidative stress, reduce hepatic stellate cell activation that reduces myofibroblast proliferation and increasing degradation of the extracellular matrix [3,4]. Anti-fibrotic liver that is often used is ursodeoxycholic acid as a single treatment or in combination with corticosteroids has proven itself as the leading therapy in some previous studies. The working principle of ursodeoxycholic acid is not directly reduce the inflammation of the liver, but by eliminating the etiology by interrupting immune-mediated pathways [4,5]. Cholestasis can reduce Hepcidin MRNA expression and significantly down regulation of hepatic hepcidin mRNA expression. The state of cholestasis in various previous studies in animals and humans raises the stress associated with the induction of inflammatory cytokines and IL-6 [6-9].