目的:探讨高脂饮食建立的C57BL/6小鼠肥胖模型的视网膜变性的超微结构改变及其与氧化应激的关系。方法:高脂饲料喂养19wk后,小鼠分为肥胖抵抗(DIO-R)组和肥胖倾向(DIO)组,同时对照组小鼠给予基础饲料。应用光镜、透射电镜及TUNEL法检测3组小鼠视网膜超微结构的改变及凋亡情况,并应用生化方法检测视网膜的氧化和抗氧化指标。结果:与对照组及DIO-R组比较,DIO组小鼠视网膜及外核层(ONL)变薄(P<0.01);感光细胞出现凋亡及坏死,其外段视盘膜排列紊乱,部分溶解、断裂,神经节细胞体积变小,细胞质分布紊乱,核染色质固缩;TUNEL法检测结果显示,在ONL层可见较多的凋亡细胞,其细胞凋亡率显著升高(P<0.01)。与对照组比较,DIO组小鼠视网膜匀浆丙二醛(MDA)含量明显升高(P<0.01),超氧化物歧化酶(SOD)活力显著下降(P<0.05)。结论:高脂诱导的肥胖可导致C57BL/6小鼠视网膜变性及细胞凋亡,其机制可能与氧化应激有一定关系。

AIM: To investigate the relationship between retinal degeneration caused by high-fat diet induced obesity and oxidative stress in C57BL/6 mice·METHODS: Mice were fed a high-fat diet for 19 weeks and then divided into diet induced obesity-resistant(DIO-R) group and diet induced obesity(DIO) group,control group mice were fed a basal diet at the same time.The retinal ultrostructural changes were detected by light and transmission electron microscope.The cellular apoptosis was detected by TUNEL.Oxidative indices were detected by biochemical methods·RESULTS: The retinal and ONL thicknesses in DIO group were thinner than in control and DIO-R groups(P<0.01).The photoreceptors in DIO group showed characteristic features of apoptosis and necrosis;the photoreceptor disk membranes were disordered and some of them were dissolved and fractured;the retinal ganglion cell in DIO group showed smaller and condensation of nuclear chromatin and increased electron density of the cytoplasm.TUNEL staining showed apoptosis cells in ONL in DIO group increased and the percentage of apoptotic cells was much higher than in control and DIO-R groups(P<0.01).Compared with the control group,the level of malondialdehyde(MDA) increased(P<0.01) and the activity of superoxide dismutase(SOD) decreased significantly(P<0.05) in DIO group·CONCLUSION: High-fat diet induced obesity may cause retinal degeneration and cellular apotosis in C57BL/6 mice,which may be related with oxidative stress in some extent.

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中国国家自然科学基金资助项目(No.30800920);辽宁省教育厅科研基金资助项目(No.L2010558)