HGF、c-Met、MVD在子宫腺肌病异位、在位内膜中的表达及意义

Expression and significance of HGF,c-Met,MVD in ectopic and eutopic endometrium with adenomyosis

目的:研究肝细胞生长因子及其受体c-Met在子宫腺肌病患者异位内膜、在位内膜及正常子宫内膜中的表达水平,在子宫腺肌病患者血管生成中的作用,探讨HGF/c-Met与子宫腺肌病的关系及可能的发病机制。方法:采用免疫组化S-P法检测30例(增生期20例、分泌期10例)经病理诊断为子宫腺肌症患者的异位、在位内膜组织及20例正常子宫内膜组织中HGF、c-Met、MVD的表达水平。结果:HGF、c-Met在异位内膜组、在位内膜组及对照组均有表达,阳性表达率及表达强度异位内膜组及在位内膜组均高于对照组(P<0.05),异位内膜组高于在位内膜组,且各组分泌期的表达均高于增生期。MVD在异位内膜组表达最高,在位内膜组次之,对照组最低。MVD计数随着HGF和c-Met的表达增强而增加。异位内膜组和在位内膜组HGF、c-Met、MVD的表达均存在两两正相关(P<0.05),对照组HGF与c-Met、HGF与MVD的表达呈正相关,c-Met与MVD的表达不相关。结论:HGF、c-Met参与了子宫腺肌病的发生,其机制与HGF/c-Met通路促进了新生血管生成有关。

Objective：To investigate the expression of HGF and c-Met in ectopic, eutopic endometrium with adenornyosis and normal endometrium and the function of HGF, c-Met in the angiogenesis of adenomyosis, and discuss the relationship of HGF/c-Met and adenomyosis for the pos- siblemechanism. Methods： Immunohistochemical（streptavidin-peroxidase） staining was employed to detect the expression of HGF, c-Met and MVD in 30 eases with adenomyosis（20 in proliferative phase and 10 in secretory phase） proved histologically of ectopic and eutopic tissues and 20 cases（10 in proliferative and secretory phase）of normal endometrial tissues. Results： HGF and c-Met were positive in ectopic, eutopic and control groups. The positive expression rate and expression intensity of HGF and c-Met were both higher in eetopic and eutopic groups com- pared with control group （ P 〈 0.05）, but expression in secretory phase was higher than that in proliferative phase in all groups. MVD showed the highest expression in ectopic group but moderately higher in eutopic group than control group. Expression of MVD increased with the rise of expression intensity of HGF and c-Met. HGF, c-Met and MVD in ectopic and eutopic groups were correlated. In control group, expression of HGF and c-Met, HGF and MVD were correlated （ P〈0.05）, but no correlation was found in the expression of c-Met and MVD. Conclusion ： HGF and c-Met function may be involved in the development of adenomyosis by hastening angiogenesis.