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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 observe the protective effect of rosiglitazone (RSG) on ultrastructural damage of HIT-T15 cells induced by glucosamine (GLEN). Methods HIT-T15 cells were divided into normal control group, GLcN + high concentration glucose culture group, GLcN + high concentration glucose + RSG 10 ~ (-6) mol / L culture group and high concentration of GLcN + Glucose + RSG10 ~ (-8) mol / L culture group. Each group was cultured for 48 hours. TEM observation of mitochondrial ultrastructure in HIT-T15 cells. Results HIT-T15 cells were observed under transmission electron microscope. Apoptotic cells and more necrotic cells were observed in GLcN group. Most of the mitochondria were unclear, some mitochondria were swollen, and pericytes widen the pathological changes of vacuolar degeneration of the endoplasmic reticulum. The ultrastructural changes of HIT-T15 cells in 10 ~ (-8) mol / L RSG group were significantly reduced compared with RSG 10 ~ (-8) mol / L group Significant change. Conclusion Glucosamine can damage the ultrastructure of islet β cell line HIT-T15 cells, Rosiglitazone can partially prevent this damage.