Department of Pathology, Faculty of Basic Medical Sciences, Kunming Medical University, 1168 West Chunrong Road, Kunming, PR China.
J Neuroinflammation. 2013 Jul 2;10:79. doi: 10.1186/1742-2094-10-79.
The effect of primary blast exposure on the brain is widely reported but its effects on the eye remains unclear. Here, we aim to examine the effects of primary blast exposure on the retina.
Adult male Sprague-Dawley rats were exposed to primary blast high and low injury and sacrificed at 24 h, 72 h, and 2 weeks post injury. The retina was subjected to western analysis for vascular endothelial growth factor (VEGF), aquaporin-4 (AQP4), glutamine synthethase (GS), inducible nitric oxide synthase (NOS), endothelial NOS, neuronal NOS and nestin expression; ELISA analysis for cytokines and chemokines; and immunofluorescence for glial fibrillary acidic protein (GFAP)/VEGF, GFAP/AQP4, GFAP/nestin, GS/AQP4, lectin/iNOS, and TUNEL.
The retina showed a blast severity-dependent increase in VEGF, iNOS, eNOS, nNOS, and nestin expression with corresponding increases in inflammatory cytokines and chemokines. There was also increased AQP4 expression and retinal thickness after primary blast exposure that was severity-dependent. Finally, a significant increase in TUNEL+ and Caspase-3+ cells was observed. These changes were observed at 24 h post-injury and sustained up to 2 weeks post injury.
Primary blast resulted in severity-dependent pathological changes in the retina, manifested by the increased expression of a variety of proteins involved in inflammation, edema, and apoptosis. These changes were observed immediately after blast exposure and sustained up to 2 weeks suggesting acute and chronic injury mechanisms. These changes were most obvious in the astrocytes and Müller cells and suggest important roles for these cells in retina pathophysiology after blast.
原发性爆炸冲击对大脑的影响已被广泛报道，但对眼睛的影响尚不清楚。在这里，我们旨在研究原发性爆炸冲击对视网膜的影响。
成年雄性 Sprague-Dawley 大鼠接受原发性爆炸高低伤暴露，并在伤后 24 小时、72 小时和 2 周时处死。对视网膜进行 Western 分析，检测血管内皮生长因子（VEGF）、水通道蛋白-4（AQP4）、谷氨酰胺合成酶（GS）、诱导型一氧化氮合酶（NOS）、内皮型 NOS、神经元型 NOS 和巢蛋白的表达；ELISA 分析细胞因子和趋化因子；免疫荧光检测胶质纤维酸性蛋白（GFAP）/VEGF、GFAP/AQP4、GFAP/巢蛋白、GS/AQP4、凝集素/iNOS 和 TUNEL。
视网膜表现出与爆炸严重程度相关的 VEGF、iNOS、eNOS、nNOS 和巢蛋白表达增加，同时伴有炎症细胞因子和趋化因子的增加。原发性爆炸暴露后还观察到 AQP4 表达和视网膜厚度增加，且与严重程度相关。最后，观察到 TUNEL+和 Caspase-3+细胞明显增加。这些变化在伤后 24 小时即可观察到，并持续至伤后 2 周。
原发性爆炸导致视网膜出现严重程度依赖性的病理变化，表现为多种参与炎症、水肿和细胞凋亡的蛋白表达增加。这些变化在爆炸暴露后立即发生，并持续至 2 周，提示存在急性和慢性损伤机制。这些变化在星形胶质细胞和 Müller 细胞中最为明显，提示这些细胞在爆炸后视网膜病理生理学中起重要作用。
