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目的探讨急性高血糖对脑缺血大鼠血-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(HMGB1)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HMGB1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HMGB1的释放,加重BBB损伤。抑制HMGB1的活性,对高血糖大鼠脑缺血后BBB的损伤具有保护作用。
Objective To investigate the effect and mechanism of acute hyperglycemia on blood-brain barrier (BBB) injury in rats with cerebral ischemia. Methods The experimental rats were randomly divided into sham operation group, normal blood glucose (NG) group, NG + GL group, hyperglycemia (HG) group and GL (HG + GL) group. The cerebrospinal fluid levels of high mobility group box 1 (HMGB1), BBB permeability, brain edema and infarct volume were measured at different time points after cerebral ischemia-reperfusion to evaluate the neurological deficits. Results Compared with NG group, the content of HMGB1 in cerebrospinal fluid of HG group was significantly increased (P <0.01). At the same time, the evacuation rate of Evans blue (EB), volume of cerebral infarction and cerebral edema significantly increased (P <0.01) (P <0.05). After GL intervention, the above indexes were significantly improved (P <0.01). Conclusion Hyperglycemia can promote the release of HMGB1 in ischemic brain tissue and aggravate BBB injury. Inhibit the activity of HMGB1 and protect the BBB after cerebral ischemia in hyperglycemic rats.