方法：实验分为AMD组、白内障组和正常组，运用生物信息学预测出AT1R是miR-410的靶基因，将正常的RPE细胞模拟AMD和白内障的微环境进行培养，检测其中miR-410的表达量，进一步将miR-410 mimics转染入细胞中，分别运用Q-PCR和Western blot的方法检测AT1R mRNA和蛋白的表达量，并通过双荧光素酶报告基因实验验证miR-410与AT1R的相互作用关系。

结果：AMD组与白内障组和正常对照组相比，RPE细胞中的miR-410表达量显著降低(P=0.0006，0.0008)，双荧光素酶报告基因实验表明，miR-410对AT1R具有明显的调控作用，且miR-410 mimics的下调效率大致为40%左右。细胞实验显示miR-410对AT1R的mRNA和蛋白表达的抑制率约为40%～50%。

结论：AT1R是miR-410的靶基因，且在AMD的RPE细胞中提高miR-410的表达可以抑制AT1R的表达。

METHODS: The experiment was divided into AMD patients, cataract patients and normal people group. AT1R was the target gene of miR-410 by bioinformatics, and the normal RPE cells were cultured in the simulated microenvironment of AMD and cataracts and the expression of miR-410 was detected. Then miR-410 mimics was transfected into cells, and the expression of mRNA and protein of AT1R were detected by Q-PCR and Western blot respectively. The relationship between miR-410 and AT1R was confirmed by the dual luciferase reporter assay.

RESULTS: The miR-410 expression of in RPE cells with AMD was significantly reduced(P=0.0006, 0.0008)compared with cataract and normal controls. The miR-410 can regulate the function of AT1R by dual luciferase reporter gene experiment and the inhibition rate was about 40%. In addition, miR-410 inhibition rate was about 40%-50% to AT1R mRNA and protein expression by cell experiment.

CONCLUSION: AT1R was a target gene of miR-410 in cell experiments, and it is demonstrated that increasing the expression of miR-410 in RPE cells with AMD can suppress the expression of AT1R.