摘要来源： bmc补体。 2020年11月10日； 20（1）：338。 EPUB 2020 11月10日。pmid： 33167932“> 33167932 Jorn-Hon Liu, Hwai-Tzong Pan, Hsin-May Lin, Hsiao-Ming Chao Howard Wen-Haur Chao BACKGROUND: Emodin has been proved to have an anti-ischemic effect on the brain, however little research has been done on its effect关于威胁性视网膜缺血。因此，对假设进行了调查l efficacy of emodin against retinal ischemia and the role ofβ-catenin/VEGF in its therapeutic mechanism. METHODS: Retinal ischemia, followed by reperfusion (IR), was inducted by raising the intraocular pressure of a Wistar rats eye to 120 mmHg 60分钟。此外，用视网膜缺血在眼睛上进行了缺血前/缺血后的静脉内注射（4、10和20μM）或媒介物。 MTT assay, electroretinograms, cresyl violet staining retinal thickness measurements, and fluorogold retrograde labelling of retinal ganglion cells (RGCs) as well as Western blotting were carried out. RESULTS: Cultured RGC-5 cells subjected to oxygen glucose剥夺（OGD）用于确认EMODIN的有效浓度（给药1小时，前OGD，前EOGD EMODIN）。在0.5时观察到了最有效和最显着的（p = 0.04）剂量的前蛋白 μM（细胞活力：47.52±3.99％）与前媒介物治疗组（38.30±2.51％）相比。此外，与缺血性静脉曲张振幅的缺血诱导的降低相比，缺血诱导的降低，与静脉前+静脉前+IR+IR+IR = 0.04±0.04±0.02）。缺血后的20μM卵素也显着减弱了相关的缺血降低（IR+EM20 = 0.24±0.09）。与缺血前静脉载体（载体+IR；全视网膜厚度= 71.80±1.08μm；视网膜内部厚度= 20.97±0.85μm； RGC = 2069.12±212.82/0.17mm），具有显着性（p <0.001）的保护作用（P <0.001），也呈现了PRED-ISCOMID。通过观察甲壳虫染色的视网膜厚度（EMO20+IR：全视网膜= 170.10±0.10μm；内视网膜= 70.65±2.06μm）和逆行荧光荧光型免疫标记的RGC密度（4623.53±179.48/0.17mm）。与正常对照相比（在假手术组中，将β-catenin/VEGF与β-肌动蛋白的比率设置为1），视网膜缺血和静脉前静脉曲观后（车辆+IR+IR = 1.64±0.14/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67/7.67±arthireβ-catenin/VEGF蛋白水平（P <0.001）显着增加（P <0.001）。 However, these elevations were significantly (P = 0.02) attenuated by treatment with emodin 20 μM (Emo20 + IR = 1.00 ± 0.19/1.23 ± 0.44). CONCLUSIONS: The present results suggest that emodin might protect against retinal ischemia insulted neurons such as RGC通过显着下调在缺血期间发生的β-catenin/VEGF蛋白的上调。