Expression of Bcl-2, Smac and their correlation in endometriosis

Abstract

Objective: To explore the expression of anti-apoptotic gene Bcl-2 and second mitochondria-derived activator of caspases (Smac) in endometriosis, the relationship of Bcl-2 and Smac with clinical staging and menstrual cycle, as well as correlation analysis.

Methods: Thirty samples of endometrial tissues taken from endometriosis patients were chosen as the study group (endometriosis group), including 16 cases in the proliferative phase and 14 cases in the secretory phase. Thirty samples of normal endometrial tissues were chosen as the control group. Immunohistochemical method (SP) was used to determine the expression of Bcl-2 and Smac proteins in each group. Statistical analysis was carried out with SPSS 16.0 statistical package. The comparison of measurement data between two groups was made by use of chi-square (χ²) test, and the correlation test of two indexes was performed by use of Spearman’s correlation analysis. The difference in statistical data was of statistical significance (p < .05).

Results: The expression of Bcl-2 in eutopic and ectopic endometrial tissues in the endometriosis group was significantly higher than that in normal endometrial tissues in the control group, and the difference was statistically significant (p < .05). The difference of Bcl-2 expression in all phases of both eutopic tissues in the endometriosis group and normal endometrial tissues was statistically significant (p < .05), the positive expression in the secretory phase was obviously lower than that in the proliferative phase. The expression intensity of Smac in eutopic and ectopic endometrial tissues in the endometriosis group was lower than that in normal endometrial tissues in the control group, and the difference was of statistical significance (p < .05). The expression intensity of Smac in ectopic endometrial tissues was lower than that in eutopic endometrial tissues, and the difference was of statistical significance (p < .05); the expression intensity of Smac in the secretory phase was higher than that in the proliferative phase in normal endometrial tissues (p < .05). The expression of Bcl-2 and Smac was not related to clinical staging of endometriosis (p > .05). The expression of Bcl-2 was negatively correlated to the expression of Smac (p < .05).

Conclusions: The high expression of Bcl-2 and the low expression of Smac enhance the abilities of hyperplasia and antiapoptosis of ectopic endometrial cells, which leads to the occurrence and development of endometriosis.