■比较有和没有贝伐单抗(BEV)和曲安奈德(TA)的猪的视网膜分支静脉阻塞(BRVO)后的基因表达变化。
■在四组九只猪(2、6、10和20天)的双眼中产生光血栓BRVO。在每一组中,六只猪一只眼睛接受了BEV的玻璃体内注射,另一只眼睛接受了TA注射,三只猪作为未经治疗的BRVO对照。三只未处理的猪作为健康对照。血管内皮生长因子(VEGF)mRNA的表达胶质纤维酸性蛋白(GFAP),肌营养不良蛋白(DMD),钾向内整流通道亚家族J成员10蛋白(Kir4.1,KCNJ10),水通道蛋白-4(AQP4),基质细胞衍生因子-1α(CXCL12),白细胞介素-6(IL6),白细胞介素-8(IL8),单核细胞趋化蛋白-1(CCL2),细胞间粘附分子1(ICAM1),通过定量逆转录聚合酶链反应分析热休克因子1(HSF1)。通过免疫组织化学表征视网膜VEGF蛋白水平。
■在未经治疗的眼睛中,BRVO显著增加GFAP的表达,IL8、CCL2、ICAM1、HSF1和AQP4。VEGF的表达,KCNJ10和CXCL12在BRVO后6天显着减少,表达在第20天恢复至健康对照水平。用BEV或TA治疗显著增加VEGF,DMD,与未经治疗的BRVO眼相比,IL6表达和抑制BRVO诱导的CCL2和AQP4上调,以及KCNJ10表达的恢复,在BRVO后10到20天。
■炎症和细胞渗透稳态而不是VEGF抑制似乎在BRVO诱导的视网膜神经变性中起重要作用,在BEV和TA处理的视网膜中增强。
■在这种BRVO急性模型中看到的内部视网膜神经变性似乎是由炎症和渗透稳态的改变而不是VEGF抑制介导的,这可能对BRVO急性期更具体的治疗方式有影响。
UNASSIGNED: To compare gene expression changes following branch retinal vein occlusion (BRVO) in the pig with and without bevacizumab (BEV) and triamcinolone acetonide (TA).
UNASSIGNED: Photothrombotic BRVOs were created in both eyes of four groups of nine pigs (2, 6, 10, and 20 days). In each group, six pigs received intravitreal injections of BEV in one eye and TA in the fellow eye, with three pigs serving as untreated BRVO controls. Three untreated pigs served as healthy controls. Expression of mRNA of vascular endothelial growth factor (VEGF), glial fibrillary acidic protein (GFAP), dystrophin (DMD), potassium inwardly rectifying channel subfamily J member 10 protein (Kir4.1, KCNJ10), aquaporin-4 (AQP4), stromal cell-derived factor-1α (CXCL12), interleukin-6 (IL6), interleukin-8 (IL8), monocyte chemoattractant protein-1 (CCL2), intercellular adhesion molecule 1 (ICAM1), and heat shock factor 1 (HSF1) were analyzed by quantitative reverse-transcription polymerase chain reaction. Retinal VEGF protein levels were characterized by immunohistochemistry.
UNASSIGNED: In untreated eyes, BRVO significantly increased expression of GFAP, IL8, CCL2, ICAM1, HSF1, and AQP4. Expression of VEGF, KCNJ10, and CXCL12 was significantly reduced by 6 days post-BRVO, with expression recovering to healthy control levels by day 20. Treatment with BEV or TA significantly increased VEGF, DMD, and IL6 expression compared with untreated BRVO eyes and suppressed BRVO-induced CCL2 and AQP4 upregulation, as well as recovery of KCNJ10 expression, at 10 to 20 days post-BRVO.
UNASSIGNED: Inflammation and cellular osmohomeostasis rather than VEGF suppression appear to play important roles in BRVO-induced retinal neurodegeneration, enhanced in both BEV- and TA-treated retinas.
UNASSIGNED: Inner retinal neurodegeneration seen in this acute model of BRVO appears to be mediated by inflammation and alterations in osmohomeostasis rather than VEGF inhibition, which may have implications for more specific treatment modalities in the acute phase of BRVO.