纤溶酶原激活、抑制因子在PCOS卵巢中的表达
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摘要
目的:研究纤溶酶原激活因子(t-PA、u-PA)及其抑制因子(PAI-1)在多囊卵巢综合征(PCOS)卵巢组织中的表达及与排卵、性激素的相关性,探讨它们在PCOS排卵障碍中的作用机制。
方法:采集PCOS患者卵巢30例及正常卵巢活检标本20例,用化学发光法检测血清性激素水平、免疫组化方法检测t-PA、u-PA及PAI-1的表达。
结果:1.PCOS组u-PA、t-PA在颗粒细胞和卵泡膜细胞的染色比正常对照组明显减弱(P＜0.05),而在间质细胞中的染色强度与正常对照组均无显著性差异(P＞0.05)
2.PCOS组PAI-1在卵泡膜细胞及间质细胞上的染色均比正常对照组明显增强(P＜0.05)。
3.PCOS组LH、LH/FSH和T均高于对照组,PAI-1与LH/FSH、T均呈正相关,u-PA、t-PA与LH/FSH、T均呈负相关。
结论:1.u-PA、t-PA及其抑制剂PAI-1相互作用、相互调节,共同作用于卵巢,调节卵泡的生长、发育与成熟。
2.PCOS患者卵巢组织中u-PA、t-PA及PAI-1的异常表达,可能是导致PCOS排卵障碍的重要因素之一。
3.卵巢PCOS组LH、LH/FSH和T均高于对照组,u-PA、t-PA、PAI-1与LH/FSH、T均相关,可能受LH、FSH及T调控。
To investigate the expression of t-PA,u-PA and PAI-1 in the ovaries of the patients with polycystic ovarian syndrome(PCOS) and the relationship between them and the female hormones,to explain further the mechanism the failure of follicular development for plasminogen activator system in PCOS.
Methods:Collecting a bit of ovary of 30patients with PCOS and 20 control patients,detecting the expression of t-PA,u-PA and PAI-1 with immuno histochemistry.
Result 1.Immunostaining of u-PA,t-PA and PAI-1 in the granulosa theca cells of PCOS were obviously weaker than that of normal control (P＜0.05).
2.Immunostaining of PAI-1 in the theca interstitial theca cells of PCOS was obviously stronger than that of normal control(P＜0.05).
3.The mean level of serum LH,LH/FSH and T of PCOS patients was higher than the control patients(P＞0.05).
Conclusion:1.The disruption of plasminogen activator system may be involved in the pathogenesis of growth and maturity offollicle.
2.The disruption of plasminogen activator system may be involved in the pathogenesis of PCOS can not ovulate.
3.Female hormones and PAI-1 perhaps adjust each other and their abnomal regulation may cause PCOS.
方法:采集PCOS患者卵巢30例及正常卵巢活检标本20例,用化学发光法检测血清性激素水平、免疫组化方法检测t-PA、u-PA及PAI-1的表达。
结果:1.PCOS组u-PA、t-PA在颗粒细胞和卵泡膜细胞的染色比正常对照组明显减弱(P＜0.05),而在间质细胞中的染色强度与正常对照组均无显著性差异(P＞0.05)
2.PCOS组PAI-1在卵泡膜细胞及间质细胞上的染色均比正常对照组明显增强(P＜0.05)。
3.PCOS组LH、LH/FSH和T均高于对照组,PAI-1与LH/FSH、T均呈正相关,u-PA、t-PA与LH/FSH、T均呈负相关。
结论:1.u-PA、t-PA及其抑制剂PAI-1相互作用、相互调节,共同作用于卵巢,调节卵泡的生长、发育与成熟。
2.PCOS患者卵巢组织中u-PA、t-PA及PAI-1的异常表达,可能是导致PCOS排卵障碍的重要因素之一。
3.卵巢PCOS组LH、LH/FSH和T均高于对照组,u-PA、t-PA、PAI-1与LH/FSH、T均相关,可能受LH、FSH及T调控。
To investigate the expression of t-PA,u-PA and PAI-1 in the ovaries of the patients with polycystic ovarian syndrome(PCOS) and the relationship between them and the female hormones,to explain further the mechanism the failure of follicular development for plasminogen activator system in PCOS.
Methods:Collecting a bit of ovary of 30patients with PCOS and 20 control patients,detecting the expression of t-PA,u-PA and PAI-1 with immuno histochemistry.
Result 1.Immunostaining of u-PA,t-PA and PAI-1 in the granulosa theca cells of PCOS were obviously weaker than that of normal control (P＜0.05).
2.Immunostaining of PAI-1 in the theca interstitial theca cells of PCOS was obviously stronger than that of normal control(P＜0.05).
3.The mean level of serum LH,LH/FSH and T of PCOS patients was higher than the control patients(P＞0.05).
Conclusion:1.The disruption of plasminogen activator system may be involved in the pathogenesis of growth and maturity offollicle.
2.The disruption of plasminogen activator system may be involved in the pathogenesis of PCOS can not ovulate.
3.Female hormones and PAI-1 perhaps adjust each other and their abnomal regulation may cause PCOS.
引文
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[2]Kolvunem R,laatikainen T,Tomes C,et al.The prevalence of Polyeystic ovaries in healthy women.Acta Obetet Gynecol Scand,1999,78(2):137-141
[3]曹泽毅.中华妇产科学(第二版).北京:人民卫生出版社,2003:2177
[4]Epifano O,Riminucci M,Manna C,et al.In vitro production of plasminogen activator by human granulosa cells.J Clin Endocrinol Metab.1994,78(1):174-179.
[5]Johnson AL,Bridgham JT,Anthony RV.Expression of avian urokinase and tissue-type plasminogen activator messenger ribonucleic acid during follicle development and atresia.Biol Reprod.1997,56(3):581-588
[6]Liu K,Feng Q,Gao HJ,et al.Expression and regulation of plasminogen activators,plasminogen activator inhibitor type-1,and steroidogenic acute regulatory protein in the rhesus monkey corpus luteum.Endocrinology.2003,144(8):3611-3617
[7]郑兴龙,龚汉.纤溶酶原激活物与排卵的研究.国外医学计划生育分册.1993,12(1):15-17
[8]Vassalli JD,Sappino AP,Belin D.The plasminogen activator/plasmin system.J Clin Invest.1991,88(4):1067-1072v[9]Loskutoff DJ,Sawdey M,Mimuro J.Type 1 plasminogen activator inhibitor.Prog Hemost Thromb,1989,9:87-115.
[10]孙林,魏巍,关咏梅。U-PA、U-PAR和PA1-1在睾酮联合hCG致多囊卵巢大鼠中的表达与意义。生殖与避孕。2006年10月第26卷
[11]The Rotterdam ESHRE/ASRM Sponsored PCOS Consensus Workshop Group.Rivised 2003 consensus on diagnostic criteria and longterm health risked related to Polycystic ovary syndrome.Fertility and Sterility,2004,81:19-25
[12]Tarkun I,Canturk Z,Arslan BC,et al.The plasminogen activator system in young and lean women with polycystic ovary syndrome.Endocr J.2004,51(5):467- 472
[13]Liu Yi-xun,Peng Xiao-rong & Ny Tor.Tissue-speicific and time-coordinated hormone regulation of plasminogen activator inhibitor type-1 and tissue-type plasminogen activator in the rat ovary during gonadotropin-induced ovulation.Eur J Biochem.1991.195(2):549-55.
[14]丁晓芳,阳永红,李红钢,等.尿激酶型纤溶酶原激活因子在小鼠精-卵接触前通讯和体外受精中作用初探。生殖与避孕,2006,26(1):3-9.
[15]张娜,刘复权,李彦群,等.转化生长因子-α及其受体在多囊卵巢综合征大鼠中的表达.河北医科大学学报,2005.26(1):5-7.
[16]Glueck CJ,Sieve L,Zhu B,et al.Plasminogen activator inhibitor activity,4G5G polymorphism of the plasminogen activator inhibitor 1 gene,and first-trimester miscarriage inwomen with polycystic ovary syndrome.Metabolism,2006,55(3):345-52.
[17]Diamanti-Kandarakis E,Palionko G,Alexandraki K,et al.The prevalence of 4G5G polymorphism of plasminogen activator inhibitor-1(PAI-1)gene in polycystic ovary syndrome and its association with plasma PAI-1 level.Eur J Endocrinol.2004.150(6):793-8.
[18]刘以训,陈毅军,彭晓蓉.催乳素延缓hCG诱发大鼠排卵和下调纤溶酶原激活系统在卵巢中的表达.生殖与避孕。1998,18(1):12-6.
[19]赵君利,陈子江,赵跃然,等.纤溶酶原激活因子1基因启动子区4G和5G多态基因型分布及其与多囊卵巢综合征的相关性研究.中华妇产科杂志,2005,40(8):528-31.
[20]Plekhanova OS,Stepauova VV,Ratner EI,et al.Urokinase Plasminogen Activator in Injured Adventitia Increases the Number of Myofibroblasts and Augments Early Proliferation[J].J Vasc Res,2006,43(5):437-446
[21]Schneie DJ,Nordt TK,Sobel BE.Attenuated fibrinolysis and accelerated atherogenesis intype 2 diabetic patients[J].Diabetes,1993,42(1):1-7.
[22]Morange PE,Alessi MC,Verdier M,et al.PAI-1 produced ex vivo by human adipose tissue is relevant to PAI-1 blood level[J].Arterioscler Thromb Vasc Biol, 1999.19(5)1361-1365.
[23]Dewailly D,Cortet-Rudelli C,Decanter C.The Polycystic Ovary Syndrome:Reproductive aspects.In:Wass JAH and Shalet SM,eds.The Oxford Text book of Endrocrinology.UK:Oxford University Press,2003.1135-1143
[24]Webber LJ,Stubbs S,Stark J,et al.Formation and early stage of follicular growth in the primate ovary.Cancer,2003,362(16):1017-1021
[25]Sengoku K,Tamate K,Takuma N,et al.The chromosomal normality of unfertilized occytes from patients with Polycystic ovarian syndrome.Hum Reprod,1997,12(5):474-477
[26]Colin MH,Role of LH and FsH in ovarian function[J].Mol Cel Endocr,2000,161(1):25-30
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