开搏通对高糖引起肾小球内皮细胞损伤防治作用的研究  

High glucose injury to human glomerular endothelial cells:mechanism and protection.

作　　者：闫振成[1] 张建国[1] 黄庆愿[2] 朱妙珍[1] 丁涵露[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所,重庆400042 [2]第三军医大学高原医学系,重庆400038

出　　处：《重庆医学》2002年第11期1045-1047,共3页Chongqing medicine

摘　　要：目的　观察高糖状态下肾小球内皮细胞过氧化损伤与内皮细胞膜流动性改变的关系 ,并探讨开搏通对其损伤的防护及机制。方法　采用体外人肾小球内皮细胞培养 ,八木组织测量之TBA法测定脂质过氧化产物丙二醛 ,Prendergast法测定细胞膜流动性 ,Fura 2双波长荧光法检测细胞内钙离子含量的变化 ,并观察开搏通对高糖致内皮细胞损伤的治疗作用。结果　高糖对肾小球内皮细胞可致过氧化损伤 ,使细胞膜流动性明显增高 ,细胞内钙含量增加 ,随着培养时间的延长 ,糖浓度愈高 ,作用愈明显 ,而开搏通可抑制细胞内钙积聚 ,改善细胞膜流动性及减轻过氧化损伤。结论　高糖引起的内皮细胞损伤和膜流动性改变是导致糖尿病肾病发生发展的因素之一 ,开搏通可防治高糖致内皮细胞损伤 ,是治疗糖尿病肾病较理想的药物之一。Objective To observe the effect of high glucose on the injury of human glomerular endothelial cells (GEC) by lipoperoxidation and the membrane fluidity of GEC.The mechanism and protection of high glucose injury to human glmerular endothelial cells by captopril was studied.Methods The culture of human GEC was established , thiobarbituric acid fluoriphotometry was used to measured MDA,Prendergast's method was used to detect the membrane fluidity of GEC,and the i was determined by Fura 2/AM,the effect of captopril on high glucose injury GEC was observed.Result The membrane fluidity of GEC was increased significantly after high glucose caused the injury to GEC by lipid peroxidation ,as the time cultured GEC with high glucose increased,the higher the concentration of glucose ,the more significant the effect,but captopril can inhibit the concentration of I in GEC ,improve cell membrane fluidity and alleviate lipid peroxidation injury. Conclusion The increased membrane fluidity caused by the injury to GEC by lipid peroxidation in high glucose may be an etiologic factor of diabetic nephropathy,captopril may improve injury of GEC caused by high glucose and be one of perfect medication treated DN .

关 键 词：葡萄糖 内皮细胞 肾小球 脂质过氧化作用 细胞膜流动性 开搏通 

分 类 号：R587.2[医药卫生—内分泌]