The contribution and modulation of vascular endothelial growth factor for brain edema formation

本研究旨在以大鼠局灶性脑缺血为对照，研究脂肪栓塞组大鼠脑水肿形成过程中星形胶质细胞反应、水通道水通道蛋白4(AQP4)和血管内皮生长因子(Vgef)的变化规律。脑含水量增加，在颈动脉注射三油酸后2小时几乎达到最大。皮下注射三油酸甘油酯后2小时，病灶周围可见AQP4免疫阳性染色增强，但病灶中心未见AQP4免疫染色，72小时可见反应性星形胶质细胞肥大，有丝分裂。注射三油酸甘油酯后2小时，星形胶质细胞内血管内皮生长因子免疫染色增强，注射后24小时和72小时更为明显，注射后2小时基底板开始消失，注射后24小时和72小时更严重。MCAO后2 h，脑含水量未见明显增加，AQP4免疫组织化学染色未见明显变化。我们的结果表明，AQP4、血管内皮生长因子和基底板的消失参与了脂肪栓子脑水肿的形成。这些因素的调节可能导致脑水肿的治疗。

The purpose of the present study was to examine the temporal profiles of astrocytic responses, water channel aquaporin 4(AQP4) and vascular endothelial growth factor(VGEF) in the process of brain edema formation in the fat embolism model in rat, comparing to those in focal brain ischemia. Brain water increased, reaching almost maximum at 2 h after intracarotid injection of triolein. Increased AQP4 immunostaining were observed in the peri-affected area but was absent in the core of the lesion 2h after triolein injection, and reactive astrocytes with hypertrophy and mitosis were observed 72h after triolein injection. VGEF immunostaining was also increased in astrocyte 2hr after triolein injection and was more significant 24h and 72h after triolein injection.Basal lamina disappearance started to happen after 2h triolein injection and were more severe 24h and 72h after triolein injection. Neither significant increase of brain water content nor significant changes in AQP4 immunostaining were seen 2 h after MCAO. Our results indicate that AQP4, VGEF and basal lamina disappearance contribute to the brain edema formation of fat emboli. The modulation of these factors could lead the brain edema treatment.