期刊文献+

COX-2在多囊卵巢综合征患者子宫内膜的表达

Expression of cyclooxygenase-2 in endometrium of cases with polycystic ovary syndrome
原文传递
导出
摘要 目的:探讨环氧合酶-2(COX-2)在多囊卵巢综合征(PCOS)患者子宫内膜的表达及治疗后的变化。方法:选择PCOS患者(PCOS组)16例,另选择卵巢功能正常的不孕患者20例为对照组,PCOS组应用二甲双胍/达英-35治疗。所有病例均测体重指数(BMI),抽血测定女性激素六项并行75 g葡萄糖耐量试验(OGTT)和胰岛素释放试验(1RT)。于月经干净3~5天(闭经患者确认为卵泡期)刮取子宫内膜组织,采用免疫组织化学技术检测PCOS组治疗前后及对照组子宫内膜COX-2的表达。结果:PCOS组患者BMI\HOMA-IR、空腹胰岛素(I0)、75 g葡萄糖负荷后2 h胰岛素(I120)及T均明显高于家族史阴性患者(P均<0.01);PCOS组治疗前COX-2在子宫内膜的表达显著高于对照组(P<0.01),治疗后其表达明显下降(P<0.05)。结论:PCOS患者子宫内膜可能处于一种慢性炎症状态,子宫内膜COX-2过度表达可能是导致患者子宫内膜异常增生和不孕的原因之一,二甲双胍/达英-35可逆转此变化。 Objective:To explore the expression of cyclooxygenase-2(COX-2) in endometrium of patients with polycystic ovary syndrome(PCOS) and its change after treatment.Methods:16 cases with PCOS(PCOS group) and 20 infertile women with normal ovarian function(control group) were selected,the cases in PCOS group were treated with metformin/diane-35.Body mass index(BMI) was detected,blood samples were extracted to detect six kinds of sex hormones,75 g oral glucose tolerance test(OGTT) and insulin release test(IRT) were performed;the endometrial tissues were scraped at 3~5 days after menstruation was clean(at follicular phase for the cases with amenorrhea),immunohistochemical method was used to detect the expression levels of COX-2 in COS group(before and after therapy) and control group.Results:The levels of BMI/HOMA-IR,fasting insulin(I0),2-hour insulin after 75 g glucose load(I120) and testosterone in PCOS group were significantly higher than those in control group(P〈0.01);the expression level of COX-2 in COS group(before therapy) was significantly higher than that in control group(P〈0.01),after therapy,the expression level of COX-2 decreased significantly(P〈0.05).Conclusion:Chronic inflammation maybe exist in endometrium of patients with PCOS,the over-expression of COX-2 may be an potential reason for abnormal hyperplasia of endometrium and infertility,metformin/diane-35 may inhibit the change.
出处 《中国妇幼保健》 CAS 北大核心 2011年第4期494-496,共3页 Maternal and Child Health Care of China
基金 唐山市科技攻关项目〔05134614e〕
关键词 多囊卵巢综合征 子宫内膜 环氧合酶-2 二甲双胍/达英-35 Polycystic ovary syndrome Endometrium Cyclooxygenase-2 Metformin/diane-35
  • 相关文献

参考文献7

  • 1Lane DE. Polycystic ovary syndrome and its differential diagnosis [ J] . Obstet Gynecol, 2006, 61 : 125.
  • 2Dhindsa G, Bhatia R, Dhindsa M et al. Insulin resistance, insulin sensitization and inflammation in polycystic ovarian syndrome [ J] . J Postgrad Med, 2004, 50:140.
  • 3Rotterdam ESHRE/ASRM -Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long - term health risks related to polycystic ovary syndrome[J] . Fertil Steril, 2004, 81 : 19.
  • 4陈述林,罗敏.胰岛素抵抗的炎症机制[J].国外医学(内分泌学分册),2004,24(6):376-378. 被引量:21
  • 5Chishima F, Hayakawa S, Sugita K et al. Increased expression of cyclooxygenase -2 in local lesions of endometriosis patients [ J ]. Am J Reprod lrnmunol, 2002, 48:50.
  • 6Basu GD, Pathangey LB, Tinder TL et al. Mechanisms underlying the growth inhibitory effects of the cyclooxygenase - 2 inhibitor celecoxib in human breast cancer cells [J] . Breast Cancer Res, 2005, 7:R422.
  • 7Elliott JL, Hostbrd SL, Demopoulos RI et al. Endometrial adenocarcinoma and polycystic ovary syndrome:risk factors, management, and prognosis [J] .South Med J, 2001, 94:529.

二级参考文献21

  • 1Rask-Madsen C, Dominguez H, Ihlemann T, et al. Tumor necrosis factor-alpha inhibits insulin's stimulating effect on glucose uptake and endothelium-dependent vasodilation in human. Circulation, 2003, 108:1815-1821.
  • 2Dandona P, Aljada A, Mohanty P, et al. Insulin inhibits intranuclear nuclear factor κB and stimulates Iκ B in mononuclear cells in obese subjects: evidence for an anti-inflammation effect? J Clin Endocrinol Metab, 2001,86: 3257-3265.
  • 3Lagathu C, Bastard JP, Auclalr M, et al. Chronic interleukin-6 (IL-6)treatment increased IL-6 secretion and induced insúlin resistance in adipocyte: prevention by rosiglitazone. Biochem Biophys Res Commun,2003,311: 372-379.
  • 4Bruun JM, Lihn AS, Madan AK, et al. Higher production of IL-8 in visceral vs. subcutaneous adipose tissue. Implication of nonadipose cells in adipose tissue. Am J Physiol Endocrinol Metab, 2004,286:E8-E13.
  • 5Hottori Y, Matsumura M, Kasai K, et al. Vascular smooth muscle cell activation by C-reactive protein. Cardiovasc Res, 2003,58:186-195.
  • 6Ma IJ, Mao SL, Taylor KL, et al. Prevention of obesity and insulin resistance in mice lacking plasminogen activator inhibitor 1. Diabetes,2004,53:336-346.
  • 7Moon B, Kwan JJ, Duddy N, et al. Resistin inhibits glucose uptake in L6 cells independently of changes in insulin signaling and GLUT4translocation. Am J Physiol Endocrinol Metab, 2003,285:E106-E115.
  • 8Bacha F, Saad R, Gungor N, et al. Adiponectin in youth: relationship to visceral adiposity, insulin sensitivity, and beta-cell function. Diabetes Care, 2004,27:547-552.
  • 9Snehalatha C, MukeskB, SimonM ,etal. Plasma adiponectinis an independent predictor of type 2 diabetes in Asian Indians. Diabetes Care,2003,26: 3226-3229.
  • 10Krogh-MadsenR, Plomgaard P, KellerP,etal. Insulin stimulates interleukin-6 and tumor necrosis factor-alpha gene expression in human subcutaneous adipose tissue. Am J Physiol Endocrinol Metab, 2004,286:E234-E238.

共引文献20

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部