Expression And Significance Of Cyclooxygenase-2 And Matrix Metalloproteinase-2 In Endometriosis

Objectives:Endometriosis, a common disease in gynecology is characterized by strong invasiveness, wide implant and easy recurrence. Its pathogenesis is still not quite clear. In recent years, the role of some enzymes in the occurrence and development of endometriosis have already aroused many people's attention. Therefore, in the study, we observed the role of cyclooxygenase-2, matrix metalloproteinase-2, cathepsinD, Ki-67 and estrogen receptor in the pathogenesis of endometriosis by immunohistochemical method. The aim is to provide important clues for the pathogenesis of endometriosis, which would provide an objective experiment evidence for the clinical treatment in endometriosis.Methods:All specimens were collected by the department of pathology in the general hospital and the second hospital in Tianjin Medical Unverisity from 2001 to 2006. There were 37 cases of ectopic endometrium with endometfiosis in experimental group, 35 cases of eutopic endometrium without endometriosis in eutopic endometrium group and 14 cases of eutopic endometrium with carcinoma in situ of cervix in normal endometium group. All tissue were maked with these specimens and were cut into 4-um sections. The rat anti-person monoclonal antibody cyclooxygenase-2, rabbit anti-person polyclonal antibodies matrix metalloproteinase-2, cathepsinD and Ki-67, rat anti-person monoclonal antibody estrogen receptor were used by immunohistochemical staining. The data was analysed by SPSS software.Results: 1 Cyclooxygenase-2 immunoreaction was observed in 97.3% (36/37) of experimental group, in 85.7% (30/35) of eutopic endometrium group and 64.3% (9/14) of normal endometrium group.2 Matrix metalloproteinase-2 was demonstrated in 97.3% (36/37) of experimental group, in 82.9% (29/35) of eutopic endometrium group and 57.1% (8/14) of normal endometrium group.3 The positive rate of cathepsinD was 100.0% (37/37), 94.3% (33/35) and 85.7% (12/14) in experimental group, eutopic endometrium group and normal endometrium group repectively.4 The expression of Ki-67 was 36.051±9.479, 34.879±11.111 and 28.686±8.984 in experimental group, eutopic endometrium group and normal endometrium group respectively.5 The expression of estrogen receptor was 27 (73.0%) of 37 cases in experimental group, 18 (72.0%) of 25 cases in eutopic endometrium group and 8 (57.1%) of 14 cases in normal endometrium group.6 The expression of cyclooxygenase-2, matrix metalloproteinase-2, cathepsinD, Ki-67 and estrogen receptor showed no significant difference between experimental group and eutopic endometrium group (p＞0.05).7 The expression of cyclooxygenase-2, matrix metalloproteinase-2 and Ki-67 in experimental group were significantly higher than normal endometrium group (p＜0.05). But the expression of cathepsinD and estrogen receptor showed no significant difference between normal endometrium group and experimental group (p＞0.05).8 There was a great correlation between the expression of cyclooxygenase-2 and matrix metalloproteinase-2 in experimental group (p＜0.05).9 There was no correlation between the expression of cyclooxygenase-2 and Ki-67, matrix metalloproteinase-2 and Ki-67 in experimental group (p＞0.05).Conclusions:1 The high expression of cyclooxygenase-2 in endometriosis may be take part in the occurrence and development of endometriosis through promoting the proliferation of cells, angiogenesis and upregulation of inflammatory mediators in ectopic lesions.2 Matrix metalloproteinase-2 was overexpressed in endometriosis, which can make ectopic endometrial tissues have a greater capacity to invade and which may play an important role in the pathogenesis of endometriosis.3 There was a positive correlation between the expression of cyclooxygenase-2 and matrix metalloproteinase-2 in endometriosis, which may be play a cooperated role in the pathogenesis of endometriosis. But the mutual mechanism of action still needs better studying.4 The expression of Ki-67 in ectopic endometrium with endometriosis was higher than normal endometrium, so the proliferative ability of ectopic endometrium was enhanced. Which indicated the ectopic endometrium with patients of endometriosis have stronger ability to implant and survive.5 The expression of cathepsinD and estrogen receptor showed no significant difference between the normal endometrium and ectopic endometrium with endometriosis, so cathepsinD and estrogen receptor may not be the main causes in the occurrence and development of endometriosis.