目的：探讨玻璃体腔注射曲安奈德(TA)对光化学诱导大鼠视网膜分支静脉阻塞(BRVO)模型血管生成及Notch通路的影响。

方法：制备光化学诱导BRVO大鼠模型，随机分为BRVO模型组、玻璃体腔注射TA后1、7、21d组； 同时设置空白对照组进行对照。眼压计测量大鼠眼压状况； 眼底彩照、荧光素眼底血管造影(FFA)和光学相干断层扫描(OCT)观察大鼠眼底情况； 蛋白免疫印迹法(WB)检测大鼠视网膜血管生成相关因子血管内皮细胞生长因子(VEGF)、血管内皮生长因子受体2(VEGFR2)，Notch通路重要因子Notch1、Jagged1、DLL4蛋白表达情况。

结果：正常对照组眼底血管排列整齐、状态清晰。BRVO模型组眼底出现水肿，视网膜变白，血管排列紊乱，视盘凹消失，视网膜血管收缩。玻璃体腔注射TA后1、7、21d组水肿逐渐减轻，血管扩张和弯曲逐渐减缓，视盘凹恢复。与空白对照组相比，BRVO模型组眼压升高，损伤处视网膜、损伤250μm处视网膜厚度增加，VEGF、VEGFR2、Notch1、Jagged1蛋白表达升高，DLL4蛋白表达降低(P<0.05)。与BRVO模型组相比，玻璃体腔注射TA后 1d组损伤250μm处视网膜厚度减少，VEGFR2、Notch1、Jagged1蛋白表达降低，DLL4蛋白表达升高； 玻璃体腔注射TA后7d组损伤处视网膜、损伤250μm处视网膜厚度减少，VEGFR2、Notch1、Jagged1蛋白表达降低，DLL4蛋白表达升高； 玻璃体腔注射TA后21d组眼压降低，损伤处视网膜、损伤250 μm处视网膜厚度减少，VEGF、VEGFR2、Notch1、Jagged1蛋白表达降低，DLL4蛋白表达升高(P<0.05)。

结论：玻璃体腔注射TA可能通过调控Notch通路抑制VEGF激活从而抑制血管生成，实现对BRVO大鼠视网膜保护作用。

METHODS: BRVO model rats were induced by photochemistry induction and randomly divided into BRVO model group and TA(1, 7, 21)d groups; at the same time, blank control group was set for comparison. The intraocular pressure of rats was measured by ophthalmotonometer; the condition of rat fundus was observed fluorescein fundus color photography(FFA)and optical coherence tomography(OCT); retinal angiogenesis related factors vascular endothelial growth factor(VEGF)and vascular endothelial growth factor receptor 2(VEGFR2), the protein expressions of Notch pathway important factors Notch 1, Jagged 1 and DLL4 were detected in rat retina by Western blotting(WB).

RESULTS: In the normal control group, the fundus vessels were arranged neatly and in a clear state. In the BRVO model group, edema appeared in the fundus, the retina turned white, the arrangement of blood vessels was disordered, the optic disc pit was disappeared, retinal vessels were in the state of vasoconstriction. In TA 1, 7 and 21d groups, edema gradually decreased, blood vessels expansion and bending gradually slowed down, and the optic disc pit was restored. Compared with the blank control group, the intraocular pressure of BRVO model group increased, the thickness of the retina increased at the injured site and 250μm far from injured site, the protein expressions of VEGF, VEGFR2, Notch1 and Jagged1 increased, the protein expression of DLL4 protein was decreased(P<0.05). Compared with the BRVO model group, in TA 1d group, the retinal thickness decreased at 250μm far from injured site, the protein expressions of VEGFR2, Notch1 and Jagged1 decreased, the protein expression of DLL4 protein increased; in TA 7d group, the retinal thickness was decreased at the injured site and 250μm far from injured site, the protein expressions of VEGFR2, Notch1 and Jagged1 decreased, the protein expression of DLL4 protein increased; the intraocular pressure of TA 21d group decreased, the thickness of the retina decreased at the injured site and 250μm far from injured site, the protein expressions of VEGF, VEGF R2, Notch1 and Jagged1 decreased, the protein expression of DLL4 protein increased(P<0.05).

CONCLUSION: Vitreous injection of TA may inhibit angiogenesis by regulating Notch pathway to inhibit the activation of VEGF, thus achieving the retinal protection in BRVO rats.