摘要目的 探讨细胞因子信号传送阻抑物(SOCS)-3和caspase-3在子宫内膜异位症中的表达及其相关性,进而了解子宫内膜异位症的发病机制.方法 采用免疫组织化学EnVision法检测32例子宫内膜异位症患者的异位内膜和在位内膜,以及30例对照组正常子宫内膜中SOCS-3和caspase-3蛋白的表达.结果 SOCS-3和caspase-3在三组子宫内膜中均有表达,且不受月经周期影响.SOCS-3在异位内膜中的评分(5.54±2.12)明显低于在位内膜(7.39±1.09,P =0.001)和对照组(7.48±1.26,P＜0.01),而在位内膜和对照组之间差异无统计学意义(p=0.756)；处于Ⅲ/Ⅳ期患者的异位内膜和在位内膜中SOCS-3表达明显低于Ⅰ/Ⅱ期(P＜0.05).caspase-3蛋白在异位内膜(3.20±1.24)和在位内膜(3.88±1.93)中的评分明显低于对照组(6.49±1.85,P＜0.01),而在位内膜和异位内膜两组之间差异无统计学意义(t=1.66,P=0.10)；不同疾病分期的caspase-3表达差异无统计学意义(P＞0.05).异位内膜中SOCS-3与caspase-3蛋白表达呈正相关(r=0.655,P＜0.01).结论 SOCS-3可能通过抑制异位子宫内膜细胞的凋亡促进子宫内膜异位症的发生发展.

abstractsObjective To investigate the expression of suppressor of cytokine signaling (SOCS)-3 and caspase-3 and their correlative significance in endometriosis.Methods Immunohistochemical EnVision method was used to detect the SOCS-3 and caspase-3 protein expression in ectopic and eutopic endometrium (n =32) of patients with endometriosis,as well as normal endometrium (n =30) of women without endometriosis.Results SOCS-3 and caspase-3 proteins were expressed in all three groups and not affected by the menstrual cycles.The expression of SOCS-3 in ectopic endometrium (5.54 ± 2.12) was significantly lower than that in eutopic (7.39 ± 1.09,P =0.001) and control group (7.48 ± 1.26,P ＜ 0.01),but without difference between the eutopic and control group (P =0.756).SOCS-3 expression in ectopic and eutopic endometrium was significantly lower in Ⅲ/Ⅳ stages than that in Ⅰ / Ⅱ stages of endometriosis (P ＜ 0.05).Significantly lower expression of caspase-3 protein was found in ectopic (3.20 ± 1.24) and eutopic endometrium (3.88 ± 1.93) as compared with the control group (6.49 ± 1.85,P ＜0.01),however ectopic and eutopic endometrium showed no significant difference (t =1.66,P =0.10).There was no significant difference of the expression of caspase-3 in ectopic and eutopic endometrium at different disease stages (P ＞0.05).Positive correlation was found between the expression of SOCS-3 and caspase-3 proteins in ectopic endometrium (r =0.655,P ＜ 0.01).Conclusion SOCS-3 may be involved in the development of endometriosis through inhibition of apoptosis of ectopic endometrial cells.