| Backgroud and aims: Hepcidin is a small molecular peptide which secreted by the liver. At present, it is already thought to be the central regulator of iron absorption and iron balance in the organism. This research is for the purpose of understanding the expression level of the hepcidin gene and its effects on iron metabolism in patients with liver cirrhosis. Methods: Using the photochmemistry law to examine 12 examples liver cirrhosis patients' as well as the healthy control individuals' serum ferritin content separately, and using the RT-PCR(reverse transcription-polymerase chain reaction) technology to examine the expression level of the hepcidin gene in liver tissues, taking actin (β-actin) as internal control. Finally, analysis the data which all obtains in the study using statistics analysis. Results: In patients with liver cirrhosis, the serum ferritin content is significantly higher than the control individuals (p<0.01). The liver hepcidin/β-actin ratio in patients with liver cirrhosis compared with control individuals is significantly higher (p<0.01) too. And the ratio correlates significantly with serum ferritin level in patients with liver cirrhosis and control individuals (p<0.01) . Conclusions: 1. Through the study found that the expression of the hepcidin gene in patients with liver cirrhosis increases significantly. Hecidin can inhibit the intestinal absorption of iron as well as the output of iron in macrophage, liver, and other tissues, and cause iron to be locked in macrophages of the reticuloendouthelial system, liver, and other tissues. That caused the circulation and utilization of iron disordered, leading to the iron content shortage in blood. At the same time, because it can inhibite the output of iron of the liver cells, so that it becomes one of the reasons that the liver can maintain the high iron content state, and the state aggravate liver injury. 2. From the results of the study ,we can have an inference that under the liver cirrhosis condition, the overloaded iron or serum ferritin of the body occupies the main status to stimulate the hepcidin secretion, and the anemia cannot display the effects on inhibiting the hepcidin secretion. |