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探讨17β-羟类固醇脱氢酶2在子宫内膜息肉中的表达及意义 被引量:2

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摘要 目的 观察和分析17β-羟类固醇脱氢酶2在子宫内膜息肉中的表达及意义。方法 选取育龄期妇女息肉组织患者30例作为观察对象,并确定为实验组;再选取正常内膜组织30例,作为对照组。采用免疫组化法测定17β-羟类固醇脱氢酶2的表达,分析研究对象月经第2-5天血清,采用电化学发光免疫分析法测定5项性激素水平,用Biosens Digital Imaging Systems图文对阳性区的积分光密度值进行测定和分析。结果 实验组增殖期和分泌期的积分光密度值分别为(43.65±4.56)和(102.45±13.5)明显低于对照组同期值(113.8±14.54)和(151.23±15.23),差异具有统计学意义(P〈0.05)。结论 宫内膜息肉组织的发生与组织局部雌性激素代谢异常有直接关系,17β-羟类固醇脱氢酶2在子宫内膜息肉中的积分光密度值下降明显可能是导致子宫内膜息肉发生的重要因素,从根本上减少宫内膜息肉的发生或再发。 b ObjectiveTo observe and analyze the 17 beta hydroxy steroid dehydrogenase 2 in the expression and signiifcance of endometrial polyps.MethodsTo select childbearing age women 30 patients with polyps group as research object, and identiifed as the experimental group;Then select 30 cases of normal endometrium tissues as control group. It was evaluated by immunohistochemical method the expression of 17 beta hydroxy steroid dehydrogenase, 2 analysis the research object serum menstruation 2-5 days, electrochemical luminescence immunity analysis method to determine the five sex hormone levels, with Biosens Digital Imaging Systems by the integral optical density of positive values are measured and analyzed.ResultsThe experimental group stage proliferation and secretion of integral optical density value respectively (43.65 ± 4.56) and (102.45 ± 13.50) signiifcantly lower than control group in the same value (113.80 ± 14.54) and (151.23 ± 15.23), and statistically signiifcant difference (P〈0.05).ConclusionIntrauterine membrane polyp group was signiifcantly associated with partial abnormal metabolism of estrogen is directly related to organization, 17 beta hydroxy steroid dehydrogenase 2 in integral optical density value decreased obviously in endometrial polyps may be an important factor to affect the occurrence of endometrial polyps, radically reduce intrauterine membrane polyp occurrence or recurrence.
作者 余瑛
出处 《当代医学》 2016年第28期2-4,共3页 Contemporary Medicine
关键词 17β-羟类固醇脱氢酶2 子宫内膜息肉 化学荧光面议 激素水平 表达 17 beta hydroxy steroid dehydrogenase 2 Endometrial polyps Chemical fuorescence negotiable Hormone levels Express
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  • 1Denger S,Reid G,Brand H,et al.Tissue-specific expression of human ER-alpha and ER- beta in male[J].Mol Cell Endocrinol,2001,178(1-2): 155-160.
  • 2Chen Z,Yuhanna IS,Gargova ZG,et al.Estrogen recepton Amediates the nongenomic activation of endothelial nitric oxide synthase by estrogen[J].J Clin Invest, 1999.103(3):401-406.
  • 3Bakir S,Mori T,Durand J,et al.Estrogen-induced vasoprotection is strogen receptor dependent:evidence from the balloon-injured rat carotid artery model[J]. Circulation,2000,101 (20): 2342-2344.
  • 4Mullick AE,Walsh BA,Reiser KM,et al. Chronic estradiol treatment attenuates stiffening,glycoxidation,and permeability in rat carotid arteries [J].Am J Physiol Heart Circ Physiol, 2001,281 (5):2204-2211.
  • 5Lindner V,Kim SK,Karas RH,et al.Increased expression of estrogen Receptor-beta mRNA in male blood vessels after vascular injury [J].Circ Res, 1998,83(2):224-229.
  • 6Brouchet L,Krust A,Dupont S,et al.Estradiol accelerates reendothelialization in mouse carotid artery through estrogen receptor-alpha but not estrogen receptor-beta[J]. Circulation, 2001,103(3):423-428.
  • 7Dubey RK,Jackson EK,Keller PJ,et al.Estradiol metabolites nhibitend othelin synthesis by an estrogen receptor-independent mechanism[J]. Hypertension,2001,37( Part 2):640-644.
  • 8Enderle MD,Sayer R,Balletshofer B,et al. Acute improvement of peripheral endothelial function in postmenopausal women with coronary artery disease after single oral intake of 17beta-estradiol valerate[J].Exp Clin Endocrinol Diabetes,2000,108(5):382-385.
  • 9Shaw L,Taggart MJ,Austin C.Mechanisms of 17 beta-oestradiol induced vasodilatation in isolated pressurized rat small arteries[J]. Br J Pharmacol,2000,129(3):555-565.
  • 10Regitz-Zagrosek V, Wintermantel TM,Schubert C.Estrogens and SERMs in coronary heart disease[J].Curr Opin Pharmacol,2007,7(2): 130-139.

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