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肾小球系膜细胞在高糖、胰岛素作用下F-actin的变化
引用本文:唐万欣,沙朝晖,黄颂敏,柳飞.肾小球系膜细胞在高糖、胰岛素作用下F-actin的变化[J].华西医学,2005,20(1):79-80.
作者姓名:唐万欣  沙朝晖  黄颂敏  柳飞
作者单位:四川大学华西医院肾内科,四川成都 610041;四川大学华西医院肾内科,四川成都 610041;四川大学华西医院肾内科,四川成都 610041;四川大学华西医院肾内科,四川成都 610041
摘    要:目的 :探讨高糖、胰岛素对肾小球系膜细胞骨架蛋白F -actin的影响 ,进一步探讨F -actin在糖尿病肾病发生发展中的作用。方法 :将培养的鼠 10 97系膜细胞分为 8组 :正常对照组 ,生理浓度胰岛素组 (10 -9M) ,低浓度胰岛素组 (10 -8M) ,高浓度胰岛素组 (10 -6M) ,高糖组 (30mM) ,甘露醇组 ,高糖加高浓度胰岛素组 ,高糖加生理浓度胰岛素组。采用rhodamine-phalloidin染色 ,激光共聚焦显微镜观察F -actin形态并测定荧光强度。结果 :高糖组F -actin荧光强度为对照组的 4 4 5 % ;10 -8M胰岛素组、 10 -6M胰岛素组分别为对照组的 12 2 4 %(P <0 0 5 )和 12 9 6 % (P <0 0 1) ;高糖加 10 -6M胰岛素组为高糖组的 183 8% (P <0 0 5 )。结论 :(1)高糖可促进F -actin解聚 ,胰岛素有一定拮抗作用 ,且呈剂量依赖性。 (2 )F -actin是糖尿病肾病发生发展中的重要因子。

关 键 词:糖尿病肾病  纤维状肌动蛋白  葡萄糖转运蛋白4  胰岛素  高糖
文章编号:1002-0179(2005)01-0079-02
收稿时间:2004-08-23
修稿时间:2004年8月23日

Effects of High Glucose Insulin on Expression of Cytoskeleton Protein F - actin of Glomerular Mesangial Cell
TANG Wan - xin, SHA Zhao- hui, HUANG Song- min,et al..Effects of High Glucose Insulin on Expression of Cytoskeleton Protein F - actin of Glomerular Mesangial Cell[J].West China Medical Journal,2005,20(1):79-80.
Authors:TANG Wan - xin  SHA Zhao- hui  HUANG Song- min  
Institution:Nephrology Department West China Hospital,Sichuan University,Chengdu 610041,China
Abstract:Objective:The effects of high glucose,insulin on cytoskeleton protein F-actin of glomerular mesangial cell(GMC)were investigated in order to explore the fuction of F-actin in the genesis and development of diabetic nephropathy (DN).Methods:Cultured 1097 rat GMC were divided into 8 groups:control,10 -9 M insulin,10 -8 M insulin,10 -6 M insulin,high glucose,mannitol,high glucose and 10 -6 M insulin,high glucose and 10 -9 M insulin.F-actin was stained by rhodamine-pholloidin and the fluorescent intensity was calculated by image analysis system.Results:High glucose could decrease the fluorescent intensity of F-actin to 44.5%(P<0.01);10 -8 M insulin,10 -6 M insulin could increase to 122.4%(P<0.05),129.6%(P<0.01)in a concentration-dependent way;high glucose and 10 -9 M insulin could increase to 183.8%(P<0.05)comparing with simple high glucose group.Conclusion:1.High glucose may facilitate the depolymerization of F-actin.Insulin could partly reverse the effects caused by high glucose above.2.F-actin may be an important factor in the pathogenesis of DN.
Keywords:Diabetic Nephropathy  F-actin  Glut4  High glucose  Insulin
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