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目的:探讨胎盘11β-HSD2和母体皮质醇水平在不同的子痫前期病理状态下的表达及其可能机制。方法:收集15例早发型重度子痫前期患者(EOSPE组)、13例晚发型重度子痫前期患者(LOSPE组)和20例正常妊娠孕妇(NP组)的血清及胎盘组织,用酶化学发光分析仪检测血清中游离皮质醇的浓度,采用免疫组化超敏即用型二步法观察胎盘11β-HSD2在合体滋养层细胞的表达,采用实时荧光定量PCR法检测胎盘组织11β-HSD2的mRNA表达。结果:正常妊娠、早发型、晚发型重度子痫前期组的血清游离皮质醇水平分别为(728.05±155.91)nmol/L、(619.80±180.57)nmol/L、(750.53±153.80)nmol/L,组间比较差异无统计学意义(P>0.05)。免疫组化胎盘11β-HSD2测量平均光密度值正常妊娠、早发型、晚发型重度子痫前期组分别为0.12±0.06、0.07±0.02、0.08±0.04,组间比较差异有统计学意义(P<0.05)。实时荧光定量PCR测量胎盘11β-HSD2的mRNA表达水平在早发型、晚发型重度子痫前期组和正常妊娠组分别为:3.16±1.21、4.86±1.43、5.23±2.20,组间比较差异有统计学意义(P<0.05)。结论:胎盘11β-HSD2可能灭活皮质醇从而保护胎儿,11β-HSD2表达减少与SPE发病有关。
Objective: To investigate the expression of 11β-HSD2 and maternal cortisol in different preeclampsia pathological conditions and its possible mechanism. Methods: Serum and placental tissue were collected from 15 early-onset severe preeclampsia patients (EOSPE group), 13 late-onset severe preeclampsia patients (LOSPE group) and 20 normal pregnant women (NP group) The concentration of free cortisol in serum was detected by analyzer. The expression of 11β-HSD2 in syncytiotrophoblasts was observed by immunohistochemical two-step hypersensitivity and real-time fluorescent quantitative PCR to detect the mRNA of 11β-HSD2 in placenta expression. Results: Serum free Cortisol level in normal pregnancy, early-onset and late-onset severe preeclampsia were (728.05 ± 155.91) nmol / L and (619.80 ± 180.57) nmol / L and 750.53 ± 153.80 nmol / There was no significant difference between the two groups (P> 0.05). Immunohistochemical placental 11β-HSD2 measured average optical density value of normal pregnancy, early-onset, late-onset severe preeclampsia were 0.12 ± 0.06,0.07 ± 0.02,0.08 ± 0.04, the difference was statistically significant (P < 0.05). Real-time quantitative PCR assay of placental 11β-HSD2 mRNA expression in early-onset, late-onset severe pre-eclampsia group and normal pregnancy group were: 3.16 ± 1.21,4.86 ± 1.43,5.23 ± 2.20, the difference between the two groups was statistically significant Significance (P <0.05). Conclusion: Placental 11β-HSD2 may inactivate cortisol to protect the fetus. The decreased expression of 11β-HSD2 is associated with the pathogenesis of SPE.