Deng Jiangshan, Zhao Fei, Yu Xiaoyan, Zhao Yuwu, Li Dawei, Shi Hong, Sun Yongning
Department of Neurology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China.
PLoS One. 2014 Sep 29;9(9):e107022. doi: 10.1371/journal.pone.0107022. eCollection 2014.
Hypoglycemia-induced brain edema is a severe clinical event that often results in death. The mechanisms by which hypoglycemia induces brain edema are unclear.
In a hypoglycemic injury model established in adult rats, brain edema was verified by measuring brain water content and visualizing water accumulation using hematoxylin and eosin staining. Temporal expression of aquaporin 4 (AQP4) and the integrity of the blood-brain barrier (BBB) were evaluated. We assessed the distribution and expression of AQP4 following glucose deprivation in astrocyte cultures.
Brain edema was induced immediately after severe hypoglycemia but continued to progress even after recovery from hypoglycemia. Upregulation of AQP4 expression and moderate breakdown of the BBB were observed 24 h after recovery. In vitro, significant redistribution of AQP4 to the plasma membrane was induced following 6 h glucose deprivation.
Hypoglycemia-induced brain edema is caused by cytotoxic and vasogenic factors. Changes in AQP4 location and expression may play a protective role in edema resolution.
低血糖诱导的脑水肿是一种严重的临床事件，常导致死亡。低血糖诱导脑水肿的机制尚不清楚。
在成年大鼠建立的低血糖损伤模型中，通过测量脑含水量并用苏木精和伊红染色观察积水情况来验证脑水肿。评估水通道蛋白4（AQP4）的时间表达和血脑屏障（BBB）的完整性。我们在星形胶质细胞培养物中评估了葡萄糖剥夺后AQP4的分布和表达。
严重低血糖后立即诱发脑水肿，但即使在低血糖恢复后仍继续进展。低血糖恢复后24小时观察到AQP4表达上调和血脑屏障中度破坏。在体外，葡萄糖剥夺6小时后诱导AQP4向质膜的显著重新分布。
低血糖诱导的脑水肿由细胞毒性和血管源性因素引起。AQP4位置和表达的变化可能在水肿消退中起保护作用。
