【摘要】 目的　探讨妊娠高血压综合征 (妊高征 )患者胎盘组织中血红素氧合酶 (HO)活性变化与其同工酶HO 1和HO 2蛋白表达变化的相关性 ,及其在妊高征发病中的作用。方法　采用双波长分光光度法测定 30例妊高征患者 (妊高征组 )及 30例正常晚孕妇女 (对照组 )胎盘组织中的HO活性 ;采用免疫印迹法测定两组孕妇胎盘组织中的HO 1和HO 2蛋白相对表达量。结果　 (1)妊高征组HO的活性为 (0 3± 0 2 )nmol·mg-1·h-1,与对照组的 (0 5± 0 3)nmol·mg-1·h-1相比较 ,差异有极显著性(P <0 0 1) ;(2 )对照组HO 1及HO 2蛋白相对表达量分别为 0 7± 0 4和 0 8± 0 4 ,两者相比较 ,差异无显著性 (P >0 0 5 )。妊高征组胎盘组织中HO 1蛋白的相对表达量为 0 6± 0 4 ,与对照组比较 ,差异无显著性 (P >0 0 5 ) ;妊高征组HO 2蛋白的相对表达量为 0 6± 0 3,其表达明显降低 ,与对照组比较 ,差异有极显著性 (P <0 0 1)。HO活性变化与HO 2蛋白表达量结果一致。结论 (1)妊高征患者胎盘组织中HO 2的表达降低 ,HO活性下降 ,HO 2的表达与HO活性下降密切相关。 (2 )HO可能在妊高征患者胎盘组织损伤的病理生理中起重要作用。更多还原

【Abstract】 Objective To investigate the expression of heme oxygenase-1 (HO-1 ) and heme oxygenase-2 (HO-2) in placenta tissue of pregnancy induced hypertension (PIH), and the relationship between HO protein expression and enzymatic activity. Methods Protein expression was analyzed qualitatively and semi-quantitatively by Western blotting in placental tissue of PIH (PIH group, n=30) and normal late pregnant women (control group, n=30). The levels of HO enzymatic activity in placental tissue were measured with the double wavelength scanning by spectrophotometer. Results (1)Western blotting analysis demonstrated that the relative protein levels of HO-1 and HO-2 in placental samples of control group were 0.7±0.4 and 0.8±0.4 respectively, there were no significant difference between HO-1 and HO-2 protein levels (P>0.05). (2)The relative levels of HO-1 were 0.6±0.4 in PIH group, there was no significant difference from those in the control group (P>0.05); the relative levels of HO-2 protein were 0.6±0.3 in PIH group, that were obviously lower than those in the control group (P<0.01). The levels of HO enzymatic activity of PIH group were (0.3±0.2) nmol·mg -1·h -1, significantly lower than that of the control group [(0.5±0.3) nmol·mg -1·h -1](P<0.01). The levels of HO activity correlated with HO-2 protein levels. Conclusions The expression levels of HO-2 protein were decreased and HO enzymatic activity reduced in PIH group. HO may play a role in the pathophysiology of poor placental perfusion and tissue damage in placenta of PIH.更多还原