罗格列酮对葡萄糖胺诱导的HIT-T15细胞超微结构损伤的罗格列酮保护作用  

Protection of rosiglitazone against HIT-T15 cell damage induced by glucosamine

作　　者：张新霞[1] 黎瑶[2] 童南伟[1] 

机构地区：[1]四川大学华西医院内分泌科,成都610041 [2]成都医学院附属医院内分泌科

出　　处：《中国糖尿病杂志》2009年第8期625-628,共4页Chinese Journal of Diabetes

摘　　要：目的观察罗格列酮(RSG)对葡萄糖胺(GLEN)诱导的HIT-T15细胞超微结构损伤的保护作用。方法以叙利亚仓鼠胰岛β细胞株HIT-T15细胞作为研究对象,分为正常对照组、GLcN+高浓度葡萄糖培养组、GLcN+高浓度葡萄糖+RSG 10^(-6)mol/L培养组和GLcN+高浓度葡萄糖+RSG10^(-8)mol/L培养组。各组培养48小时。透射电镜下观察HIT-T15细胞线粒体超微结构。结果透射电镜下观察HIT-T15细胞,GLcN组可见凋亡细胞及较多的坏死细胞;多数线粒体模糊不清,个别线粒体有肿胀,核周隙变宽内质网空泡变性的病理变化。RSG 10^(-8)mol/L组的HIT-T15细胞超微结构病变明显减轻,与RSG 10^(-8)mol/L组比较,RSG 10^(-8)mol/L组病变无明显改变。结论葡萄糖胺可损伤胰岛β细胞株HIT-T15细胞超微结构,罗格列酮可以部分阻止这种损伤。Objective To explore the protection of rosiglitazone （RSG） against ultrastructure impairment of HIT-T15 cell induced by glueosamine. Methods β-cell line HIT-T15 cells were used and divided into four groups： （l）eontrol, （2）8mM GLcN＋11mM glucose, （3）SmM GLcN＋11mM glucose＋ RSG 10^-6 M and （4） 8mM GLcN＋ 11mM glucose＋ RSG 10^-8 M. The studies were performed on the mitochondrial uttrastructure of HIT-T15 cells and apoptosis rate： Results Transmission electron microscope showed apoptosis, necrosis and endoplasmic reticulums vaeulation in HIT-T15 ceils treated with GLcN, with characterizations of illegible and swelling mitochondrion, wide intermittent space of nuclear, and degenerated endoplasmic reticulum. The HIT-T15 cells treated with RSG 10^-8 M showed greatly improvements in the pathological alterations of ultrastructure. Less or no improvement was seen in the cells treated with RSG 10^-6 M. Conclusions Our findings have confirmed that GLeN impairs HIT-T15 ceils, while RSO protects the cellular structures against the damage in a concentration-dependent manner.

关 键 词：葡萄糖胺 罗格列酮 β细胞线粒体 超微结构 

分 类 号：R96[医药卫生—药理学]