方法：将60只3周龄C57BL/6小鼠随机分为实验组和正常对照组(NC)，包括形觉剥夺3wk组(FDM 3W，n=20)，形觉剥夺4wk组(FDM 4W，n=20)，FDM3W正常对照组(FDM 3W-NC，n=10)和FDM4W正常对照组(FDM 4W-NC，n=10)，实验组右眼遮盖，左眼自然暴露作为自身对照，正常对照组不予任何处理。在实验3wk及4wk时检测所有小鼠屈光状态，HE染色观察巩膜及视网膜组织结构变化，免疫组织化学方法及实时荧光定量PCR观察Smad1在视网膜中的表达情况。

结果：(1)自身对照眼和正常对照组呈生理性远视化发展，FDM3W、FDM4W实验眼均呈相对近视化发展，差异具有统计学意义(P<0.05)；(2)与自身对照组及正常对照组比较，FDM3W、FDM4W实验眼巩膜及视网膜明显变薄； 实验眼视网膜中Smad1表达明显下降，差异具有显著统计学意义(P<0.01)。

结论：小鼠形觉剥夺性近视眼视网膜(尤其是内核层及内丛状层)中Smad1的表达呈下调趋势，Smad1极有可能通过转导视网膜信号参与了近视发生发展过程。

METHODS: Sixty 3-week-old C57BL/6 mice were randomly divided into experimental groups and normal groups(NC)which totally include four groups: form-deprived 3wk group(FDM3W, n=20), form-deprived 4wk group(FDM4W, n=20), FDM3W normal control group(FDM3W-NC, n=10)and FDM4W normal control group(FDM4W-NC, n=10). Mice in experimental groups were treated with diffuser wearing on right eyes(MD-T), and their left eyes were naturally exposed as their self-control group(MD-C). The normal control groups were free of all the treatments, but the same measurements were performed at the same time-point. Refractive status was examined at 3 and 4wk after treatments in all mice. The histological analysis was applied to assess the changes of the sclera and the retina. The immunohistochemical staining and quantitative real-time PCR(QRT-PCR)were applied to investigate the expression of Smad1 protein and mRNA in retina.

RESULTS:(1)There was no significant difference between right and left eyes in every group before experiment. The normal control eyes showed physiological farsighted development and the MD eyes demonstrated relatively myopization. After experiments, a significant myopia shift had been induced in MD-T compared with MD-C and NC(P<0.05).(2)Histopathologic examination showed posterior sclera and retina in MD-T were thinner than in MD-C and NC groups. Compared with MD-C and NC groups, the expression of Smad1 in retina in MD-T was significantly decreased(P<0.01).

CONCLUSION:The expression of Smad1 in retina of form-deprived myopia was down-regulated, and Smad1 likely to be involved in the development of myopia through the transduction of retinal signal.