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中文摘要：
目的探讨长期酒精暴露诱导胰岛素抵抗对小鼠血视网膜屏障的损伤以及神经鞘磷脂（SM）可能的作用。方法选取神经鞘磷脂合成酶2（SMS2）基因敲除（SMS2-/-）和野生型（WT）小鼠76只，酒精暴露建立动物模型。用血糖仪测定血糖浓度，酶联免疫法（ELISA）测定血胰岛素浓度，并计算胰岛素抵抗指数（HOMA—IR），利用免疫荧光染色、HE和电子显微镜观察血视网膜屏障的损伤。结果长期酒精暴露引起小鼠胰岛素抵抗（P〈0．05），并出现血视网膜屏障的损伤，如无细胞毛细血管数增多（P〈0．05），星形胶质细胞数量减少（P〈0．05），内皮细胞和周细胞线粒体肿胀，嵴消失，基底膜欠清晰，呈剂量依赖性。和wT小鼠相比，SMS2-/-小鼠胰岛素抵抗指数较小和血视网膜屏障损伤程度较轻（P〈0．05），提示SMS2-/-小鼠有延缓胰岛素抵抗形成和减少血视网膜屏障损伤的作用。结论长期酒精暴露可以诱导胰岛素抵抗，并造成血视网膜屏障损伤，具有剂量依赖性；SMS2基因的缺失有延缓胰岛素抵抗的产生和减少血视网膜屏障损伤的作用。
英文摘要：
Objective To investigate the mechanism of insulin resistance and retinal damages induced by long-term alcohol exposure, especially the mechanisms which SM （sphingomyelin, SM） regulationin is involved in. Methods Sphingomyelin synthase 2 knockout （SMS2-/-） mice and wild type （WT） mice were used to establish the long term alcohol exposure models. The total cases were 76 in each group. Blood glucose and blood insulin were measured with ELISA assay, in both SMS2 -/- mice and WT mice. In the meantime, homeostasis model assessment of insulin resistance （HOMA-IR） was calculated. Finally, the pathologic alterations about retinal microvasculature were investigated with immunofluorescent labeling, hematoxylin and eosin staining and electron microscopy. Results Long-term alcohol exposure induced insulin resistance with dose dependency （P 〈 0. 05 ） , and blood retinal barrier （BRB） damages, such as acellular capillaries increased （P 〈 0. 05 ） , astrocytes decreased （ P 〈 0.05 ） and damages of endothelial cell in ultrastrctural level, with dose dependency. In addition, either insulin resistance index increase or BRB damages in SMS2-/- mice were less than in WT mice （P 〈 0. 05） , suggesting SMS2 -/- mice might attenuate insulin resistance and BRB damages. Conclusion The insulin resistance （IR） and BRB damages can be induced by long-term alcohol exposure. As an oxidative stress factor,alcohol exposure may lead to the activation of PKC-NFKB-（Bcl-Xs） pathway and produce the effects of IR and BRB damages.
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