Objective To investigate the possible mechanism of rat retinal degeneration induced by sodium iodate(NaIO3) . Methods Twenty male SD rats were randomly divided into the control and model groups. The rats were given 30 mg.kg-1 NaIO3 by tail in travenous injection to establish dry age-related macular degeneration models. Twenty}ne days later, electroretinogram (ERG) and retinal histopathological changes were observed. The activity of superoxide dismutase(SOD) and catalase(CAT) and the level of malondialdehyde(MDA) in rat retina were measured. Differentially expressed proteins were analyzed by liquid chromatography-mass spectrometry. Results ERG results showed that NaIO3 treatment significantly reduced b-wave amplitudes of Scotopic; 0.01 ERG，Scotopic 3.0 ERG，Scotopic; 3.0 oscillatory potentials，Photopic 3.0 ERG，and Photopic 3.0 flash responses by 79.98%，81.64%，76.08%，61.68 % and 57.25 %，respectively(all P<0.05) . The retina in the model rats showed a reduction in cell layers and a disordered structure especidally in the outer and inner nuclear layers，compared with the control rats. Compared with the control group，the SOD and CAT activity in the model group decreased by 12.51% and 14.08%，respectively，while the MDA level increased by 57.96%(all P<0.05) . Gene ontology-based analysis revealed that the biological processes involving 80 up-regulated proteins were mainly concentrated On positive regulation of gene expression，inflammatory response，aging, and cellular response to interleukin}, and the biological processes involving 18 down-regulated proteins were focused on visual perception，response to light stimulus，and phototransduction. Kyoto encyclopedia of genes and genomes-based analysis showed that the differentially expressed proteins were enriched in phototransduction，proteasome，Janus kinase/signal transducer and activator of transcription signaling pathway，endocytosis，and complement and coagulation cascades . Conclusion NaIO3 can promote the inflammatory and immune processes through specific; oxidative stress and inhibit the phototransduction pathway in the retina，inducing retinal degeneration.

目的 探讨碘酸钠(NaIO_3)诱导大鼠视网膜退行性改变的作用机制。方法 取雄性SD大鼠20只，随机分为对照组和模型组。采用30 mg·kg~(-1) NaIO_3尾静脉注射，建立大鼠干性年龄相关性黄斑变性病变模型。继续饲养21 d,检测大鼠视网膜电图(ERG),观察大鼠视网膜组织病理学变化，检测大鼠视网膜组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和丙二醛(MDA)含量，采用液相色谱-质谱联用分析差异蛋白情况。结果 ERG检测结果显示，模型组大鼠暗适应0.01ERG、暗适应3.0ERG、暗适应3.0振荡电位以及明适应3.0ERG和明适应3.0闪烁光反应b波振幅分别比对照组降低79.98%、81.64%、76.08%、61.68%、57.25%,差异均有统计学意义(均为P<0.05)。与对照组相比，模型组大鼠视网膜组织细胞层数减少，尤其是外核层、内核层结构紊乱，呈现明显的波浪形变化。与对照组相比，模型组大鼠视网膜组织SOD和CAT活性分别下降12.51%和14.08%,MDA含量增加57.96%,差异均有统计学意义(均为P<0.05)。GO分析显示，模型组较对照组上调的80个蛋白，所参与的生物学过程在调控基因表达(positive regulation of gene expression)、炎症反应(inflammatory response)、衰老(aging)以及对白细胞介素(IL)-6的细胞反应(cellular response to interleukin-6)等方面具有显著性。18个下调蛋白参与的生物学过程非常集中，主要表现在视觉感知(visual perception)、对光刺激的反应(response to light stimulus)、光转导(phototransduction)。KEGG分析结果显示，差异蛋白主要富集于光转导(phototransduction)、蛋白酶体(proteasome)、JAK-STAT信号通路(JAK-STAT signaling pathway)、细胞内吞(endocytosis)、补体及凝血级联反应(complement and coagulation cascades)等通路。结论 NaIO_3可通过特异性氧化应激引发炎症与免疫过程，同时抑制视网膜光转导通路，诱导视网膜退行性改变。

邢岩;