妊娠高血压综合征患者胎盘组织中血红素氧合酶的表达

Expressive difference of heme oxygenase in human placenta tissue from patients with pregnancy induced hypertension

目的:探讨血红素氧合酶(HO)的2种同工酶(诱导型HO1和组织型HO2)在正常妊娠晚期和妊娠高血压综合征(妊高征)患者胎盘组织中的基因及蛋白表达。方法:采用逆转录聚合酶链反应(RTPCR)方法测定正常妊娠和妊高症患者各30例胎盘组织中HO1mRNA及HO2mRNA的表达;并采用免疫组化方法进行HO蛋白半定量分析。结果:①妊高征组HO1mRNA的相对表达量为0.34±0.18,HO2mRNA为0.88±0.57,分别与正常妊娠组(0.46±0.30和0.87±0.28)比较差异均无统计学意义(P>0.05);2组均显示HO1mRNA的表达弱于HO2mRNA。②免疫组化显示HO1在妊高征组胎盘绒毛滋养细胞和血管内皮细胞的染色分数分别为8.1±2.6和1.9±0.5,分别与正常妊娠组(9.3±2.0和2.4±0.3)比较差异均无统计学意义(P>0.05)。妊高征组HO2蛋白在胎盘血管内皮细胞的表达为4.5±2.6,明显低于正常妊娠组(6.9±3.7,P<0.05);HO2在滋养细胞的表达2组间差异无统计学意义(P>0.05)。结论:胎盘血管内皮细胞HO2表达降低可能在妊高征胎盘血管灌注不足和胎盘组织损伤的病理中发挥重要作用。

Aim： To investigate the gene and protein expression of heme oxygenase-1 （ HO-1 ） and heme oxygenase-2 （HO-2） in placenta tissue from normal pregnancy and pregnancy induced hypertension （PIH） . Methods： Reverse transcription polymerase chain reaction （RT-PCR） was used to detect the expression of HO-1 mRNA and HO-2 mRNA, and protein expression was analyzed semi-quantitatively using immunohistochemistry in placenta tissue of normal pregnancy （control group, n = 30） and PIH （PIH group, n = 30）. Results： RT-PCR analysis demonstrated that the relative mRNA levels of HO-1 and HO-2 in placental samples of PIH group were （0.34±0.18） and （0.88±0.57） which had no significant difference compared with those in control group （0.46±0.30） and （0.87±0.28 ） ,P 〉 0.05. The expression of HO-1 mRNA was lower than HO-2 mRNA in both groups. Immunohistochemistry demonstrated that the staining of HO-1 in cell of trophoblast and capillaries were （8.1±2.6） and （1.9 ±0.5 ） in PIH group, which had no significant difference compared with those in control group （9.3±2.0 ） and （2.4±0.3 ） ,P 〉 0.05 ; the staining of HO-2 protein in capillaries were （4.5±2.6 ） in PIH group, which was obviously lower compared with that in control group （6.9±3.7 ） ,P 〈 0.05 ; there was no significant difference between the staining of HO-2 protein in trophoblast in both groups. Conclusion： The decreased expression of HO- 2 protein may play a role in the pathophysiology of poor placental perfusion and tissue damage of PIH.