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作 者:行俊秀[1] 张跃辉[1] 胡敏[1] 胥风华[1] 吴效科[1] 侯丽辉[1]
机构地区:[1]黑龙江中医药大学附属第一医院妇产科,哈尔滨150040
出 处:《科技导报》2009年第4期75-79,共5页Science & Technology Review
基 金:中国-芬兰科学技术合作基金项目;国家自然科学基金项目(30572404);黑龙江省自然科学基金重点项目(ZJY0506-01)
摘 要:为了不同药物干预组的绒毛膜滋养层细胞中胰岛素受体底物-1(IRS-1)和丝裂原活化蛋白激酶(MAPK)蛋白的表达及其与妊娠期高血压的关系,采用以下方法:①体外原代培养人绒毛膜滋养细胞,用沃漫青霉素作用于滋养细胞诱发胰岛素抵抗的细胞模型;②用蛋白印迹法检测IRS-1和磷酸化细胞外信号调节激酶(p-ERK)在正常组、溶剂组、胰岛素抵抗组、丹参酮组和二甲双胍组中的变化。结果显示:①显微镜下可见细胞呈多边形,细胞平铺生长,有细胞融合后形成的合体滋养层细胞;②当细胞胰岛素抵抗时,IRS-1的GSR为0.6857,较正常对照组GSR(0.5417)升高了26.58%,加入药物改善胰岛素抵抗后,丹参酮组的GSR(0.5890)降低了16.42%,二甲双胍组的GSR(0.6429)降低了6.66%;③在沃漫青霉素诱发胰岛素抵抗时,p-ERK的GSR为1.7,较正常对照组GSR(1.0833)升高了56.93%;加入药物改善胰岛素抵抗后丹参酮组的GSR(1.3425)较抵抗组降低了26.63%,二甲双胍组的GSR(1.5429)较抵抗组降低了10.18%。由此得出结论:①丹参酮2对IRS-1的胰岛素抵抗改善水平优于二甲双胍;②丹参酮2和二甲双胍对p-ERK均有降调作用;③丹参酮2通过对IRS-1、p-ERK的调节,改善了妊娠期高血压疾病的胰岛素抵抗状态。This paper investigates the expression of mitogen- activated protein kinase and insulin receptor substrate-1 in trophoblastic cells and the relationship with hypertensive disorder complicating pregnancy. With primary culture of human placental villus in vitro, trophoblastic cells were exposed to 2.5 μmol/L wortmannin for 48 hours to establish insulin-resistant trophoblastic cell. Protein expression of insulin receptor substrate-1 and extracellular signal-regulated kinase was obtained by western blotting. Under the microscope, the polygon cell took the shape of monolayer slice and there were some syncytio-trophoblasts by cell fusion; with insulin resistance, the level of insular signal transmission of the main protein IRS-1 was risen 26.58% above the normal level. With treatment of tanshinone, it was reduced 16.42% as compared with the model. With treatment of metformin, the level of insular signal transmission of the main protein IRS-1 reduced 6.66% as compared with the model. With insulin resistance, protein expression of extracellular signal-regulated kinase was risen 56.93% above the normal level. With treatment of tanshinone, protein expression of extracellular signal-regulated kinase reduced 26.63% as compared with the model. With treatment of metformin, protein expression of extracellular signal-regulated kinase reduced 10.18% as compared with the model. It is concluded that with the trophoblastic cell in insulin resistance, the protein expression of IRS-I and p-ERK will rise. Use of tanshinone2 and metformin will reduce the protein expression of IRS-I and p-ERK.
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