机构地区:[1]上海交通大学医学院附属国际和平妇幼保健院妇产科,200030
出 处:《中华围产医学杂志》2013年第9期566-571,共6页Chinese Journal of Perinatal Medicine
摘 要:目的探讨血脂代谢异常在子痫前期发病中的可能作用。方法选择2011年11月1日至2012年6月30日存上海交通大学附属同际和平妇幼保健院剖宫产分娩的重度子痫前期孕产妇30例为重度子痫前期组,同期剖宫产分娩的正常孕产妇30例为对照组。采用逆转录-实时定量聚合酶链反应(reverse transcription-real time polymerase chain reaction,RT PCR)法检测胎盘组织巾的脂蛋白脂酶(lipoprotein lipase,LPL)及内皮脂酶(endothelial lipase,EL)mRNA的相对表达水平;Western印迹法检测胎盘组织中LPL和EL蛋白的相对表达水平;免疫组织化学方法研究LPL、EL存胎盘组织中的定位;并同时检测2组产妇血清中的血脂浓度。采用t检验及秩和检验比较上述指标在2组产妇间的差异。结果(1)与对照组比较,重度子痫前期组孕产妇血清中甘油三酯浓度增高[(2.75±0.92)mmol/L与(3.35±0.80)mmol/L,t=3.082,P=0.003]、高密度脂蛋白胆同醇浓度降低[(1.85±0.22)mmol/L与(1.64±0.34)mmol/L,t=3.157,P=0.003]及动脉硬化指数增高(2.47±0.34与2.76±0.46,t=3.066,P=0.003)。(2)重度子痫前期产妇胎盘组织中LPLmRNA相对中位表达水平高于对照组[1.26(0.46~1.58)与0.52(0.34~0.84),Z=-2.587,P-0.010],EL mRNA相对中位表达水平低于对照组[0.65(0.48~0.76)与1.32(0.94~1.62),Z=4.154,P=0.000]。(3)免疫组织化学结果显示LPL蛋白和EL蛋白均表达于母胎界面血管合体膜上直接接触母体血流的合体滋养细胞和直接接触胎儿血流的内皮细胞的胞质中。(4)重度子痫前期组孕产妇胎盘组织中LPL蛋白相对中位表达水平高于对照组[0.68(0.46~0.83)与0.31(0.15~0.55),Z=3.335,P=0.001],而EL蛋白相对中位表达水平低于对照组[0.13(0.11~0.16)与0.70(0.56~0.81),Z=-Objective To investigate the effect of abnormal lipid metabolism in the pathogenesis of preeclampsia. Methods Thirty women with severe preeclampsia who delivered by cesarean section in the International Peace Maternity & Child Health Hospital from November 1, 2011 to June 30, 2012, were included as the study group. Thirty normal pregnant women delivered during the same period by cesarean section were included as the control group. The mRNA levels of lipoprotein lipase (LPL) and endothelial lipase (El.) in the placentas were quantified by real time polymerase chain reaction. The expression of LPL/EL protein was detected by Western blot assay and the distribution on the placenta was determined by immunohistochemical staining. The maternal serum level of lipid markers was detected by automatic biochemical analyzer. Difference between the two groups was compared with t test or rank sum test. Results (2) The triglyceride (TG) concentration E(3.35 ± 0.80) mmol/l, vs (2.75 ±0.92) mmol/L, t = 3. 082, P= 0.0031 and atherosclerosis index (AI) (2.76±0.46 vs 2.47±0.34, t=3.066,P=0.003) increased in the study group compared with the control group, while the concentration of high-density lipoprotein-cbolestrol (HI)I.c) decreased[(1.64±0.34) mmol/L vs (1.85!0.22) mmol/L,z=3.157,P:0.003]. (2) The median level of LPL mRNA expression in placenta of the study group was higher than that of the control EL 26 (0.46-1.58) vs 0.52 (0.34-0.84) ,Z= 2. 587,P=0. 010], whereas the expression ofEL mRNA was lower [0.65 (0.480.76) vs 1.32 (0.94 1.62),Z= 4.154, P=0.000]. (3) Immunohistochemical analysis showed that the placenta EL and LPL located in cytoplasm of syncytiotrophoblast cells at the materno placental interface and of endothelial cells at the feto-placental interface. (4) Compared with the control group, the median level of LPL protein expression in placenta in the study group increased E0. 68(0.46-0.83) vs 0.31(0. 15 0.55),Z =3.335,P 0.001], an
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