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作 者:王冬花[1] 刘义[1] 邓小艳[1] 吕立群[1] 盛慧[1] 尹婕[1] 肖维[1] 龚成[1]
机构地区:[1]华中科技大学同济医学院附属协和医院妇产科,武汉430022
出 处:《生殖医学杂志》2007年第6期387-391,共5页Journal of Reproductive Medicine
摘 要:目的探讨黄体生成素(LH)对多囊卵巢综合征(PCOS)患者卵巢黄素化颗粒细胞胰岛素受体底物(IRS)-1和IRS-2 mRNAs及蛋白质表达的影响,其及在卵巢局部胰岛素抵抗中的作用。方法收集行体外受精-胚胎移植(IVF-ET)治疗的11例PCOS患者(PCOS组)和15例排卵正常的输卵管性不育患者(对照组)促排卵后黄素化颗粒细胞行体外培养,分别用不同浓度LH(0、20、200、2,000 mIU/ml)处理细胞48 h,采用逆转录聚合酶链反应(RT-PCR)和免疫印迹法(Western-blot)检测黄素化颗粒细胞IRS-1和IRS-2 mRNAs及蛋白质的表达。结果(1)与对照组比较,PCOS组黄素化颗粒细胞IRS-1 mRNA及蛋白质表达显著增加(P<0.05),IRS-2 mRNA及蛋白质表达显著降低(P<0.05);(2)不同浓度LH作用后,PCOS组黄素化颗粒细胞IRS-1 mRNA及蛋白质的表达显著增加,IRS-2 mRNA及蛋白质的表达变化不明显;对照组则均无显著变化。结论PCOS异常增高的LH可能通过增加黄素化颗粒细胞IRS-1 mRNA及蛋白质的表达参与了患者卵巢局部选择性胰岛素抵抗的发生。Objective: To study the effect of luteinizing hormone (LH) on insulin receptor substrate(IRS) 1 and 2 mRNAs and protein expression in ovarian luteinizing granulosa cells from patients with polycystic ovary syndrome (PCOS), and to explore the roles of the abnormal increasing LH in ovary insulin resistance in PCOS. Methods: Ovarian luteinizing granulosa cells from PCOS patients (n=11) and normally ovulating controls (n=15) were obtained in the process of IVF-ET, and treated with different concentrations of LH (0, 20, 200, or 2,000 mIU/ml)for 48 h. mRNAs of IRS-1, IRS-2 in ovarian luteinizing granulose cells were assessed by semi-quantitative RT-PCR. The protein expressions of insulin IRS-1, IRS-2 in ovarian luteinizing granulose cells were analyzed by Western blot. Results: (1) As compared with those in control group, luteinizing granulose cells in PCOS patients had higher IRS-1 mRNA and protein expression (P 〈 0. 05), but lower IRS-2 mRNA and protein expression (P〈0. 05). (2) LH significantly increased the IRS-1 mRNA and the protein expression in luteinizing granulose cells in patients with PCOS, but had no effect on IRS-2 mRNA and protein expression. There was no effect of LH on IRS-1 and IRS-2 mRNAs and protein expression in luteinizing granulose cells in normally ovulating women. Conclusion: Elevated LH may participate in the selective insulin resistance of PCOS by up-regulating IRS-1 mRNA and protein expression.
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