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目的 研究罗格列酮 (RSG)对胰岛素抵抗 (IR)大鼠 β细胞超微结构病变的作用。 方法高糖饲料喂养SD大鼠 6周复制IR大鼠模型。成模后用药组予RSG 10 μmol·kg-1·d-1,用药 6周。未用药IR大鼠模型为对照 (IR组 )。透射电镜观察胰岛 β细胞超微结构。 结果 与IR组相比 ,RSG组大鼠收缩压、血清甘油三酯、游离脂肪酸、胰岛素降低 (均P <0 .0 1) ,胰岛素敏感指数、血清高密度脂蛋白胆固醇升高 (均P <0 .0 1)。电镜观察IR大鼠 β细胞可见凋亡早期改变 ,细胞浆内脂质沉积以及细胞核和细胞器的病理变化。RSG组 β细胞超微结构病变明显减轻 ,未见凋亡的 β细胞及胞浆内脂质沉积。 结论 罗格列酮可有效防治高糖饲料诱导IR大鼠 β细胞的病理损害
Objective To study the effect of rosiglitazone (RSG) on β-cell ultrastructure in insulin resistance (IR) rats. Methods High glucose diet was used to induce IR rat model of SD rats for 6 weeks. The rats in the model group received RSG 10 μmol · kg-1 · d-1 for 6 weeks. The untreated IR rat model served as a control (IR group). Transmission electron microscope observation of islet β cell ultrastructure. Results Compared with IR group, the systolic blood pressure, serum triglyceride, free fatty acid, insulin (P <0.01), insulin sensitivity index and serum high density lipoprotein cholesterol increased significantly in RSG group (all P < 0 .0 1). Electron microscopy of IR rat β cells showed early changes in apoptosis, intracellular plasma lipid deposition and changes in the pathological changes of the nucleus and organelles. The ultrastructural changes of β cells in RSG group were significantly reduced, and no apoptotic β cells and intracellular lipid deposition were observed. Conclusion Rosiglitazone can effectively prevent and treat β-cell pathological damage induced by high glucose in IR rats