sEng、NO在妊娠期高血压疾病患者血清中表达水平及意义
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摘要
目的:探讨sEng与NO在妊娠期高血压疾病发病中的作用,了解sEng在正常妊娠不同阶段血清中表达水平。
方法:选择妊娠期高血压疾病患者30例为实验组(妊娠期高血压组5例、子痫前期轻度组8例,子痫前期重度组17例),同期正常妊娠妇女50例为对照组(早孕、中孕妇女各10例,晚孕妇女30例)。采用酶联免疫吸附试验(ELASA)测定血清sEng表达水平,硝酸盐还原酶法测定血清NO表达水平。
结果:
1.sEng、NO在正常妊娠不同阶段血清中的表达:
(1)sEng在正常早、中、晚孕组血清中表达水平分别为0.78±0.22 ng/ml、1.83±0.49 ng/ml、3.65±0.49 ng/ml,早孕组低于中孕组和晚孕组,差异有统计学意义(P＜0.05),中孕组低于晚孕组,差异有统计学意义(P＜0.05);
(2)NO在正常早、中、晚孕组血清中表达水平分别为34.39±7.52μmol/L、73.46±6.18μmol/L、78.17±8.09μmol/L,早孕组低于中孕组和晚孕组,差异有统计学意义(P＜0.05),中孕组低于晚孕组,但两组比较无统计学差异(P＞0.05)。
2.sEng、NO在妊娠期高血压疾病组血清中的表达:
(1)sEng在妊娠期高血压组、子痫前期轻度组、子痫前期重度组血清中表达水平分别为4.81±0.81 ng/ml、5.63±0.90 ng/ml、6.80±1.21 ng/ml,妊娠期高血压组高于正常晚孕组(P＜0.05);子痫前期轻度组高于妊娠期高血压组,但两组比较无统计学差异(P＞0.05);子痫前期重度组高于子痫前期轻度组、妊娠期高血压组,差异均有统计学意义(P＜0.05)。
(2)NO在妊娠期高血压组、子痫前期轻、重度组血清中表达水平分别为59.07±9.19μmol/L、54.73±11.77μmol/L、41.13±8.05μmol/L,妊娠期高血压组明显低于正常晚孕组,差异有统计学意义(P＜0.05),子痫前期轻度组低于妊娠期高血压组,但差异无统计学意义(P＞0.05),子痫前期重度组低于子痫前期轻度组、妊娠期高血压组,差异有统计学意义(P＜0.05)。
3.妊娠期高血压疾病组血清sEng水平与NO水平呈显著负相关关系(r=-0.66,P＜0.01)。
结论:
1.妊娠期高血压疾病患者血清sEng表达水平升高、NO表达水平降低,二者升高与降低水平与病情轻重关系密切;
2.血清中高表达水平的sEng可能通过降低血清NO表达水平参与妊娠期高血压疾病的发生发展。
Objective:To investigate the role of sEng/NO in the pathogenesis of hypertensive disorder complicating pregnancy.To detect the sEng levels in serum of normal pregnant at different trimester.
Methods:Choose 30 patients with hypertensive disorder complicating pregnancy(gestational hypertension 5 cases,mild preeclampsia 8 cases,severe preeclampsia 17 cases),normal pregnant women 50 cases(the first trimester 10 cases,the second trimester 10 cases,the third trimester 30 cases).Quantikine human sEng enzymelinked immunoassay(ELISA)kits were used to detect the serum level of sEng, the serum level of NO were detected by nitrite reductase kits.
Results:
1.The sEng levels and the NO levels in serum of normal pregnant at different trimester:
(1)The sEng levels in serum of the first trimester group、the second trimester group and the third trimester group were 0.78±0.22 ng/ml、1.83±0.49 ng/ml、3.65±0.49 ng/ml,respectively.The sEng levels in the first trimester group lower than those in the second trimester group(P＜0.05), the second trimester group lower than the third trimester group(P＜0.05);
(2)The NO levels in serum of the first trimester group、the second trimester group and the third trimester group were 34.39±7.52μmol/L、73.46±6.18μmol/L、78.17±8.09μmol/L,respectively.NO levels in the first trimester lower than the second trimester(P＜0.05),the second trimester lower than the third trimester(P＞0.05).
2.The sEng levels and the NO levels in serum of the patients with hypertensive disorder complicating pregnancy:
(1)The sEng levels in serum of the gestational hypertension group、the mild preeclamsia group and the sever preeclampsia group were 4.81±0.81 ng/ml、5.63±0.90 ng/ml、6.80±1.21 ng/ml,respectively,the gestational hypertension group were significantly higher than those in the normal third trimester group(P＜0.05),the mild preeclamsia group were higher than the gestational hypertension group,but had no significant different(P＞0.05).The sever preeclampsia group were significantly higher than the mild preeclamsia group and the gestational hypertension group (P＜0.05).
(2)The NO levels in serum of the gestational hypertension group、the mild preeclamsia group and the sever preeclampsia group were 59.07±9.19μmol/L、54.73±11.77μmol/L、41.13±8.05μmol/L, respectively.The gestational hypertension were significantly lower than those in the normal third trimester group(P＜0.05).The severe preeclampsia group were significant lower than the mild preeclampsia (P＜0.05),there were no significant different between the mild preeclampsia group and the gestational hypertension group(P＞0.05).
3.sEng levels were correlated positively with NO levels(r=-0.66, P＜0.01)in the patients with hypertensive disorder complicating pregnancy.
Conclusions:
1.The sEng levels increased and the NO levels decreased in patients with hypertensive disorder complicating pregnancy,the two factors correlates with disease severity.
2.High sEng levels in serum may step down the NO levels then play a role in the pathophysiology of hypertensive disorder complicating pregnancy.
方法:选择妊娠期高血压疾病患者30例为实验组(妊娠期高血压组5例、子痫前期轻度组8例,子痫前期重度组17例),同期正常妊娠妇女50例为对照组(早孕、中孕妇女各10例,晚孕妇女30例)。采用酶联免疫吸附试验(ELASA)测定血清sEng表达水平,硝酸盐还原酶法测定血清NO表达水平。
结果:
1.sEng、NO在正常妊娠不同阶段血清中的表达:
(1)sEng在正常早、中、晚孕组血清中表达水平分别为0.78±0.22 ng/ml、1.83±0.49 ng/ml、3.65±0.49 ng/ml,早孕组低于中孕组和晚孕组,差异有统计学意义(P＜0.05),中孕组低于晚孕组,差异有统计学意义(P＜0.05);
(2)NO在正常早、中、晚孕组血清中表达水平分别为34.39±7.52μmol/L、73.46±6.18μmol/L、78.17±8.09μmol/L,早孕组低于中孕组和晚孕组,差异有统计学意义(P＜0.05),中孕组低于晚孕组,但两组比较无统计学差异(P＞0.05)。
2.sEng、NO在妊娠期高血压疾病组血清中的表达:
(1)sEng在妊娠期高血压组、子痫前期轻度组、子痫前期重度组血清中表达水平分别为4.81±0.81 ng/ml、5.63±0.90 ng/ml、6.80±1.21 ng/ml,妊娠期高血压组高于正常晚孕组(P＜0.05);子痫前期轻度组高于妊娠期高血压组,但两组比较无统计学差异(P＞0.05);子痫前期重度组高于子痫前期轻度组、妊娠期高血压组,差异均有统计学意义(P＜0.05)。
(2)NO在妊娠期高血压组、子痫前期轻、重度组血清中表达水平分别为59.07±9.19μmol/L、54.73±11.77μmol/L、41.13±8.05μmol/L,妊娠期高血压组明显低于正常晚孕组,差异有统计学意义(P＜0.05),子痫前期轻度组低于妊娠期高血压组,但差异无统计学意义(P＞0.05),子痫前期重度组低于子痫前期轻度组、妊娠期高血压组,差异有统计学意义(P＜0.05)。
3.妊娠期高血压疾病组血清sEng水平与NO水平呈显著负相关关系(r=-0.66,P＜0.01)。
结论:
1.妊娠期高血压疾病患者血清sEng表达水平升高、NO表达水平降低,二者升高与降低水平与病情轻重关系密切;
2.血清中高表达水平的sEng可能通过降低血清NO表达水平参与妊娠期高血压疾病的发生发展。
Objective:To investigate the role of sEng/NO in the pathogenesis of hypertensive disorder complicating pregnancy.To detect the sEng levels in serum of normal pregnant at different trimester.
Methods:Choose 30 patients with hypertensive disorder complicating pregnancy(gestational hypertension 5 cases,mild preeclampsia 8 cases,severe preeclampsia 17 cases),normal pregnant women 50 cases(the first trimester 10 cases,the second trimester 10 cases,the third trimester 30 cases).Quantikine human sEng enzymelinked immunoassay(ELISA)kits were used to detect the serum level of sEng, the serum level of NO were detected by nitrite reductase kits.
Results:
1.The sEng levels and the NO levels in serum of normal pregnant at different trimester:
(1)The sEng levels in serum of the first trimester group、the second trimester group and the third trimester group were 0.78±0.22 ng/ml、1.83±0.49 ng/ml、3.65±0.49 ng/ml,respectively.The sEng levels in the first trimester group lower than those in the second trimester group(P＜0.05), the second trimester group lower than the third trimester group(P＜0.05);
(2)The NO levels in serum of the first trimester group、the second trimester group and the third trimester group were 34.39±7.52μmol/L、73.46±6.18μmol/L、78.17±8.09μmol/L,respectively.NO levels in the first trimester lower than the second trimester(P＜0.05),the second trimester lower than the third trimester(P＞0.05).
2.The sEng levels and the NO levels in serum of the patients with hypertensive disorder complicating pregnancy:
(1)The sEng levels in serum of the gestational hypertension group、the mild preeclamsia group and the sever preeclampsia group were 4.81±0.81 ng/ml、5.63±0.90 ng/ml、6.80±1.21 ng/ml,respectively,the gestational hypertension group were significantly higher than those in the normal third trimester group(P＜0.05),the mild preeclamsia group were higher than the gestational hypertension group,but had no significant different(P＞0.05).The sever preeclampsia group were significantly higher than the mild preeclamsia group and the gestational hypertension group (P＜0.05).
(2)The NO levels in serum of the gestational hypertension group、the mild preeclamsia group and the sever preeclampsia group were 59.07±9.19μmol/L、54.73±11.77μmol/L、41.13±8.05μmol/L, respectively.The gestational hypertension were significantly lower than those in the normal third trimester group(P＜0.05).The severe preeclampsia group were significant lower than the mild preeclampsia (P＜0.05),there were no significant different between the mild preeclampsia group and the gestational hypertension group(P＞0.05).
3.sEng levels were correlated positively with NO levels(r=-0.66, P＜0.01)in the patients with hypertensive disorder complicating pregnancy.
Conclusions:
1.The sEng levels increased and the NO levels decreased in patients with hypertensive disorder complicating pregnancy,the two factors correlates with disease severity.
2.High sEng levels in serum may step down the NO levels then play a role in the pathophysiology of hypertensive disorder complicating pregnancy.
引文
[1]乐杰.妇产科学《第六版》.人民卫生出版社,2004,97-104.
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[4]Levine RJ,Maynard SE,Qian C,et al.Circulating angiogenic factors and the risk of preeclampsia[J].N Engl J Med,2004,350:672-683
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[1]乐杰.妇产科学《第六版》.人民卫生出版社,2004,97-104.
[2]Sibai B,Dekker G,Kupferminc,M,et al.Pre-eclampsia[J].Lancet,2005,365(9461),785-799.
[3]Maynard S,Epstein FH,Karumanchi SA,et al.Preeclampsia and angiogenic imbalance[J].Annu Rev Med.2008;59:61-78.
[4]Levine RJ,Maynard SE,Qian C,et al.Circulating angiogenic factors and the risk of preeclampsia[J].N Engl J Med,2004,350:672-683
[5]Teppa RJ,Ness RB,Crombleholme WE,et al.Free leptin is increased in normal pregnancy and further increased in preeclampsia[J].Metabolism,2000,49:1043-1048.
[6]Venkatesha S,Toporsian M,LamC,et al.Soluble endoglin contributes to the pathogenesis of preeclampsia[J].Nat Med,2006,12(6):642-649.
[7]Levine R J,Lam C,Qian C,et al.Soluble Endoglin and Other Circulating Antiangiogenic Factors in Preeclampsia[J].N Engl J Med.2006,355(10):992-1005.
[8]Li C,Hampson IN,Hampson L,et al.CD105 antagonizes the inhibitory signaling of transforming growth factorβ1 on human vascular endothelial cells[J].FASEBJ,2000,14:55.
[9]Li DY,Sorensen LK,Brooke BS,et al.Defective angiogenesis in mice lacking endoglin[J].Science.1999,284,1534-1537.
[10]Toporsian M,Gros R,Kabir MG,et al.A role for endoglin in coupling eNOS activity and regulating vascular tone revealed in hereditary hemorrhagic telangiectasia[J].Circ Res,2005,96(6):684-92.
[11]Diez-Marques L,Ortega-Velazquez R,Langa C,et al.Expression of endoglin in human mesangial cells:modulation of extrascellular matrix synthesis[J].Biochimica et Biophysica Acta,2002,1587:36.
[12]Sanehez-Elsner T,Botella LM,Velasco B,et al.Endoglin expression is regulated by transcriptional cooperation between the hypoxia and transforming growth factor-beta pathways[J]. J Biol Chem. 2002;277:43799-43808.
[13]Romero R, Nien JK, Espinoza J, A longitudinal study of angiogenic (placental growth factor) and anti-angiogenic (soluble endoglin and soluble vascular endothelial growth factor receptor-1) factors in normal pregnancy and patients destined to develop preeclampsia and delivery a small for gestational age neonate. J Matern Fetal Neonatal Med[J]. 2008,21(1):9-23.
[14]Anthony FW,Evans PW,Wheeler T, et al. Variation in detection of VEGF in maternal serum by immunoassay and the possible influence of binding proteins[ J]. Ann Clin Biochem, 1997,34: 276-280.
[15]Torry DS,Wang HS,Wang TH, et al.Preeclampsia is associated with reduced serum levels of placenta growth factor [J].Am J Obstet Gynecol, 1998,179: 1539-1544.
[16]Romero R, Nien JK, Espinoza J, A longitudinal study of angiogenic (placental growth factor) and anti-angiogenic (soluble endoglin and soluble vascular endothelial growth factor receptor-1) factors in normal pregnancy and patients destined to develop preeclampsia and delivery a small for gestational age neonate[J]. J Matern Fetal Neonatal Med. 2008,21(1):9-23.
[17]Gu Y, Lewis DF, Wang Y. Placental productions and expressions of soluble endoglin, soluble fms-like tyrosine kinase receptor-1, and placental growth factor in normal and preeclamptic pregnancies[J]. J Clin Endocrinol Metab. 2008 Jan;93 (1):260-6.
[18] Robinson CJ, Johnson DD. Soluble endoglin as a second-trimester marker for preeclampsia[J]. Am J Obstet Gynecol 2007;197:174.el-5.
[19] Logolo AF,Nonogaki S,Miguel RE,et al.Transferming growth factor-beta expression in head and neck squamous cel curcinoma patients as re-lated to prognosis[J].J Oral Pathol Med,2003,32(3):139-145.
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