| Background:The stem cell is a kind of cell which can keep alive for a long term and has a few of differentiation potencies. While,the progenitor cell is a kind of cell keeping one or double ways of differentiation and the capability of its differentiation,self-renew and self-maintenance is confined. For the survival time,the progenitor cell is shorter than the stem cell. As the researching results,hepatic stem cells can be found in the adult liver,the oval cell,As progenitor cell,can differentiate into hepatocyte and bile duct epithelium cell. Because the oval cell can take part in hepatic tissue repair,the study on the hepatic stem cell has become a researching topic in the world. If the disorder repair for the hepatic injury means possible carcinomatous change,does the oval cell take part in the formation of the hepatic cellular cancer (HCC)? which is not clear. Where does the hepatic stem cell originate and locate ? The question is not clear too. In order to interpret the questions,the animal model of HCC will be established in the experiment.Objective:The aim of the experiment is to search for the regulation that the hepatic stem cells abnormally differentiate into cancer cells. In the experiment,the variating regulation of PCNA,c-kit and c-myc in the formation and development of HCC will be interpreted with immunohistochemistry and RT-PCR. So,the initial mechanism that hepatic stem cells abnormally differentiate into cancer cells from the levels of cell,protein and gene will be clarified. The last,the inhibition to HCC with ulinastain will be studied,from which,a new way of clinical prevention and treatment for HCC will expect to be explored. Methods and Results1. The animals were divided into three groups which are HCC inducing group (Group A),interference group (Group B) and control group (Group C). Group A and Group B were ate DAB forage,and ulinastain was injected from abdominal cavity in Group B. The results showed that DAB is a HCC inducer which is simple,cheap and effective. In the 16th and 20th week,the incidence rate of HCC in Group B was 25% and 50% respectively,and which was lower than that of Group A.2. The developing process of HCC can be divided into three periods:the period of inflammation (Period I),the period of fibrosis (Period II) and theperiod of cancer (Period III). The oval cells were found in the portal area in the early of Period I . The more serious of hepatic injury,the more oval cells were found. In the Period II and Period III,the oval cells can migrate into hepatic loubfe and can be found in the cancer nodule.3. The expression of c-kit and PCNA was detected by immunohistoche-mistry. The protein encoded by c-kit gene was fistly found in the portal area in the Period II,and in this period,the oval cells were obviously positive stained. With the hepatic injury becoming more serious and with the liver cancer forming,and most of positive cells still located in the portal area. Furthermore,some positive cells could be found in the hepatic lobule and cancer nodule. The expression of PCNA located in the nucleus,and the oval cells in the portal area were only positively stained in the early of Period I. In the metaphase of Period I,a great deal of hepatocytes showed positive expression. In this period,the quantity of the positive cells was most in the process of HCC information. In the Period II,the quantity of the positive cells was fewer than before,and in the Period III,it rose again.4. The expressing level of c-myc mRNA was detected with RT-PCR. And which showed a raising tendency in the process of HCC formation,and the intervention of ulinastain was no effect for it.Conclusion1. In the early period of hepatic injury,the oval cells were found in bile duct epithelial lining in the portal area. With the hepatic injury becoming more serious and hyperplasia of the liver fiber,the oval cells migrated into the hepatic lobufe going along the liver fiber. In the Period III,the oval cells were found in the cancer nodule and in the margin. On the whole,the oval c...
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