In the last decade, advances in the understanding of genes promoting hepatic stellate cell (HSC) activation are impressive. However, there are few breakthroughs in therapeutic intervention of hepatic fibrogenesis. Efficient and well-tolerated antifibrotic drugs are lacking and current treatment of hepatic fibrosis is limited to withdrawal of the noxious agent. Research identifying innocuous antifibrotic agents is of high priority and urgently needed. Emodin is efficacious in the management of hepatic fibrosis. However, the mechanisms underlying its effects remain to be elucidated.
A research team from China established rat models of experimental hepatic fibrosis by injection with CCl4; the treated rats received emodin via oral administration at a dosage of 20 mg/kg twice a week at the same time. Rats injected with olive oil served as a normal group. Histopathological changes were observed by hematoxylin and eosin staining. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and hepatic hydroxyproline content were assayed by biochemical analyses. The mRNA and protein relevant to hepatic stellate cell (HSC) activation in the liver were assessed using real-time reverse transcription-polymerase chain reaction, immunohistochemistry, western blotting and enzyme-linked immunosorbent assay. Their study will be published on October 14, 2009 in the World Journal of Gastroenterology.