实验性大鼠肝脏癌变过程中生长抑素受体2表达的意义

目的：研究生长抑素受体2（SSTR2）在肝癌癌变过程中的表达和分布，探讨SSTR2在肝癌发生过程的作用。方法：二乙基亚硝胺溶液(DENA)诱发SD大鼠发生肝癌，RT-PCR和免疫组化检测肝硬化肝组织、肝癌中SSTR2的mRNA和蛋白表达，比较不同时期肝组织中SSTR2-mRNA和蛋白的表达。结果：DENA诱癌8周后，可见肝癌形成。诱癌8周时，癌旁肝组织SSTR2-mRNA明显高于正常肝脏（1.794±0.212 vs 0.950±0.138,P<0.05），随着诱癌时间的延长，SSTR2-mRNA的表达逐渐增强，到16周时到最高（2.053±0.169），随后逐步下降（22周时低至1.468±0.107），而肝癌组织SSTR2-mRNA表达只为1.219±0.249。免疫组化检测SSTR2蛋白表达发现，SSTR2主要位于胞浆和细胞膜，SSTR2蛋白表达的变化与SSTR2-mRNA的变化一致。结论：SSTR2在实验性肝硬化早期表达逐步升高，随着肝硬化的加重和肝细胞癌变的发生，SSTR2表达逐渐下降。SSTR2表达下降可能与肝细胞癌发生、发展密切相关。

Significance of somatostatin receptor 2 expression in the murine liver tissue during carcinogenesis

AIM：To study the expression and distribution of somatostatin receptor 2 (SSTR2) during carcinogenesis of hepatocellular carcinoma (HCC) and to evaluate the role of SSTR2 in the carcinogenesis of HCC.METHODS：Experimental HCC model was induced in SD rats using EDNA.SSTR2 mRNA and protein expression were detected by RT-PCR and immunohistochemistry.SSTR2 expression in different tissues at different periods of carcinogenesis were compared.RESULTS：HCC nodule developed after 8 weeks of administration of EDNA.Semi-quantitative analysis showed that SSTR2-mRNA expression in cirrhotic liver tissue at 8 weeks of induction was significantly higher than that in normal liver tissue (1.794±0.212 vs 0.950±0.138,P<0.05).As induction prolonged,SSTR2-mRNA expression increased,and reached its peak level of 2.053±0.169.Then,it decreased gradually.At 22 weeks,SSTR2-mRNA expression decreased to 1.468±0.107,which was significantly lower than the values at 8 weeks and 16 weeks (P<0.05).SSTR2-mRNA in HCC tissue was at low expression level with an average of 1.219±0.249.SSTR2 protein expression was mainly at cytosol and membrane.The change of SSTR2 protein expression in different tissue was consistent with the change of mRNA expression.CONCLUSION：SSTR2 expression was increased at early stage of cirrhosis.At the late stage of cirrhosis and occurrence of HCC,SSTR2 expression was significantly decreased.Down-regulation of SSTR2 may contribute to the carcinogenesis and progression of HCC.