MMP-2、TIMP-2和PPARγ在子痫前期患者胎盘中的表达及意义

Expression and significance of MMP-2,TIMP-2 and PPARγ in placenta of patients with preeclampsia

目的探讨MMP-2、TIMP-2和PPARγ在子痫前期患者胎盘中的表达及其临床意义。方法采用免疫组化SP法检测正常妊娠晚期、轻度子痫前期及重度子痫前期各30例患者胎盘底板中间型滋养细胞MMP-2、TIMP-2及PPARγ的表达。结果 MMP-2在正常妊娠晚期组、轻度子痫前期组及重度子痫前期组的表达强度呈减弱趋势,在重度子痫前期组的表达明显低于正常妊娠晚期组及轻度子痫前期组(P<0.05);TIMP-2、PPARγ在正常妊娠晚期组、轻度子痫前期组及重度子痫前期组的表达强度呈增强趋势,各组间差异有显著性(P<0.05);子痫前期组患者胎盘组织中MMP-2、TIMP-2及PPARγ的表达呈负相关(P<0.05)。结论子痫前期组患者胎盘组织中MMP-2表达下调,TIMP-2、PPARγ表达上调,提示MMP-2、TIMP-2和PPARγ的表达异常可能在滋养细胞的浸润过程中起主导作用;MMP-2、TIMP-2及PPARγ的表达呈负相关,提示三者可能在滋养细胞浸润过程中相互影响,共同参与子痫前期的发病。

Purpose To investigate the expression and clinical significance of MMP-2, TIMP-2 and PPARγ in placenta of patients with preeclampsia. Methods Placenta tissues were collected from the normal-term pregnancy group （ n = 30）, the mild preeclampsia group （n =30） and the severe preeclampsia group （n = 30）. Immunohistochemistry （SP） was used to detect the expressions of MMP-2, TIMP-2 and PPARγ in intermediate trophoblast of placental floor. Results The expression level of MMP-2 in the severe preeclampsia group was obviously lower than that in the mild preeclampsia group （ P 〈 0. 05 ）. The expression of MMP-2 had a decreasing tendency from the normal-term pregnancy group to the severe preeclampsia group. The expression levels of TIMP-2 and PPARγ in normal-term pregnancy group, the light preeclampsia group and the severe preeclampsia group had an increasing tendency, the difference between the groups was significant （ P 〈 0. 05 ）. The expression of MMP-2 with TIMP-2 and PPARγ in placenta of patients with preeclampsia was negatively correlated （ P 〈 0. 05 ）. Conclusion Down-regulation of MMP-2 expression and up-regulation of TIMP-2 and PPARγ in the placenta of patients with preeclampsia suggest that the abnormal expression of MMP-2, TIMP-2 and PPARγ may be correlated to the incidence of preeelampsia. The negative correlation between expression of MMP-2 with TIMP-2 and PPAR＇y in placenta of patients with preeclampsia may suggest that MMP-2, TIMP-2 and PPARγ affect one another in the process of trophoblast invasion and participate in the pathogenesis of preeclampsia together.