中文摘要：

目的探讨急性高血糖对脑缺血大鼠血一脑脊液屏障（BBB）损伤的作用及机制。方法实验大鼠随机分为假手术组、正常血糖（NG）组、加甘草酸（GL）（NG＋GL）组、高血糖（HG）组和加GL（HG＋GL）组。于脑缺血再灌注不同时间段检测脑脊液高迁移率族蛋白B1（HMGBl）含量、BBB通透性、脑水肿和脑梗死体积，评估神经缺失。结果与NG组比较，HG组大鼠的脑脊液HMGBl含量显著提高（P〈0．01）；同时，伊文思蓝（EB）外渗率，脑梗死体积及脑水肿显著加重（P〈0．01），神经功能缺陷加重（P〈0．05）；进行GL干预后，上述指标显著改善（P〈0．01）。结论高血糖可促进缺血脑组织HMGBl的释放，加重BBB损伤。抑制HMGBI的活性，对高血糖大鼠脑缺血后BBB的损伤具有保护作用。

英文摘要：

Objective To investigate the effects of acute hyperglycemia on ischemia-induced blood-brain barrier （BBB） impairment and the mechanism involved. Methods Wistar rats were randomly divided into sham operation group, normoglycemia （NG） group, hyperglycemia （HG） group and glycyrrhizic acid （GL） intervention （ NG ＋ GL, HG ＋ GL） groups. Ischemia was induced by 90 minutes middle cerebral artery occlusion. Western blotting was used to detect the release of high mobility group box 1 （ HMGB1 ） in cerebrospinal fluid, and BBB permeability was evaluated by Evan＇s blue （EB） leakage. Brain edema, infarction volume, neurological deficit scores were evaluated after opera- tion. Results Hyperglycemia significantly enhanced the release of HMGB1 in cerebrospinal fluid, compared with the NG group （ P 〈 0.01 ）. Meanwhile, Hyperglycemia significantly increased the brain edema and the infarction volume （ P 〈 0.01 ） and worsened the neurological deficit （ P 〈 0.05 ）. Inhibition of HMGB1 with GL significantly reduced EB leakage, brain edema, infarction volume, and neurological deficit （P 〈 0.01 ）. Conclusion In transient middle cere- bral artery occlusion, the increased release of HMGB1 may contribute to the hyperglycemia-exacerbated BBB damage. Inhibiting HMGB1 may protect the BBB from the hyperglycemia-exacerbated damage.