Hepatic fibrosis is thought to be a reversible disease, however, there is no satisfactory method in clinical practice to reverse the pathological process yet . Several drugs, including antisense TGF 1 receptors, cytokines , antioxidants, chemical drugs , soluble type ? receptor of TGF 1, and TGF 1 antibodies have been used in research work to block experimental hepatic fibrosis, but their effects were not as prosperous as we had expected. Some traditional Chinese drugs have been found effective in preventing fibrogenesis and other causes of chronic liver injury , and this helps to develop a more hopeful future in controlling liver fibrosis and cirrhosis. Emodin is a main active monomer isolated from Giant Knotweed Rhizome, which is widely used in traditional Chinese herb treatment of liver cirrhosis . It is easy to extract, isolate and identify emodin, so it shows excellent prospects in the development of some new drugs for treating hepatic fibrosis. CCl4, a highly toxic chemical agent, causes hepatic injury including hepatocytic necrosis, steatosis, and inflammation. Research for establishing a model of liver fibrosis with CCl4 began in 1936.
Since then many methods to establish a model of liver fibrosis have been tried . Among them, Nutlin-3 selleck hepatic fibrosis caused by CCl4 has been extensively used in experimental models in rats because hepatic responses in rats to chronic CCl4 stimulation are shown to be superficially similar to human cirrhosis . Hepatocyte damage is the initial factor of hepatic fibrogenesis and activities of ALT and AST in serum are the most commonly used biochemical markers of liver injuries . Hydroxyproline is an amino acid found almost exclusively in collagens. Determination of the content of hydroxyproline in liver tissue is regarded as a good method to quantify fibrosis and to evaluate the effectiveness of new potentially antifibrotic agents. In this study, the method of subcutaneously injecting CCl4 was used to establish the model of liver fibrosis. Histological analysis showed CCl4 caused prominent hepatic steatosis, necrosis, and formation of regenerative nodules and fibrotic septa between the nodules.
Biochemical assay showed serum ALT activities, serum AST activities, and content of hepatic Beta-catenin inhibitor hydroxyproline were markedly increased in rats injected with CCl4 for 12 wk, which are consistent with the histological observations. Our results suggest that oral administration of edomin daily for 12 wk improved the state of steatosis with a significant reduction in the number of macro and microvesicular steatosis, and it also apparently suppressed hepatic fibrogenesis by reducing the thickness of bridging fibrotic septa. Emodin could decrease the scores of hepatic fibrosis grading, inhibit the ALT and AST activities in serum and reduced the content of hepatic hydroxyproline.