慢性肝炎和原发性肝癌患者血管生成素的表达比较及其与血管生成之间的关系

目的探讨原发性肝癌和慢性肝炎组织中血管生成素-1（Ang-1）、血管生成素-2（Ang-2）的表达与血管生成间的关系。方法应用免疫组织化学方法对26例原发性肝癌组织以及58例慢性肝炎组织中Ang-1、Ang-2及CD34标记的微血管密度（MVD）进行检测。结果原发性肝癌组织中Ang-2表达明显高于慢性肝炎组织，差异有显著性（P〈0．05）；而Ang-1在两组间比较无显著性差异（P〉0．05）。原发性肝癌组织中MVD水平明显高于慢性肝炎组织，两组比较差异有显著性（P〈0．05）。相关性分析表明，Ang-2与原发性肝癌肿瘤大小、分级、有无转移、MVD水平相关。慢性肝炎组织中Ang-1、Ang-2表达随着炎症程度分级和纤维化程度分期越高表达越强，但将各分期合并为不同的组合后，各组间比较无显著性差异（P〉0．05）。结论血管生成在慢性肝炎发展到肝癌中起重要作用，但Ang-1、Ang-2作为一种重要的血管生成因子，其在促进慢性肝炎发展到肝癌中的证据还不是很充分，机制还有待进一步研究。

Comparison in the expression of the angiopoietin between chronic hepatitis and primary carcinoma patients and its association with angiogenesis

Objective To investigate the expression of angiopointin-1 （Ang-1）,angiopointin-2 （Ang-2） in primary carcinoma of the liver（PHC） and chronic hepatitis, and the relationship in Ang-1, Ang-2 and angiogenesis. Methods The expression of Ang-1, Ang-2 in 26 PHC specimens and 58 chronic hepatitis specimens was examined by immunohistochemistry. Immunohistochemical staining of CD34 was performed to determine the microvessel density （ MVD ）. Results The expression of Ang-2 in PHC was higher than that in chronic hepatitis tissues with significant difference （ P 〈 0.05 ） ; No significant difference of Ang-1 expression in the two groups（ P 〉 0.05 ）. MVD levels in PHC tissues was significantly higher than chronic hepatitis tissues（ P 〈 0.05 ）. Correlative analysis showed that Ang-2 expression was correlated with PHC tumor size, grade, metastasis, MVD level. Higher the inflammation and fibrosis stage, stron- ger the expression of Ang-1 ,Ang-2 in Chronic hepatitis tissues. However, if the stages were combined into different combinations, no significant difference was in each group （ P 〉 0.05 ）. Conclusion Angiogenesis plays an important role in the progression of chronic hepatitis to liver cancer. As an important angiogenesis factor, the evidence for taking Ang -1 and Ang -2 as an important angiogenesis factor in the development of chronic hepatitis to liver cancer was not sufficient. The further study was expected for the mechanism.