葡萄糖胺对脑缺血再灌注损伤的保护作用

目的:观察葡萄糖胺对脑缺血再灌注损伤的保护作用,为其临床应用提供实验依据。方法:应用HT22细胞缺糖缺氧模型(oxygen-glucose dexprivation model,OGD),观察葡萄糖胺对细胞活性和乳酸脱氢酶释放率的影响。制备小鼠大脑中动脉栓塞模型(middle cerebral artery occlusion,MCAO),缺血2 h拔线再灌注前尾静脉注射葡萄糖胺(0.1、0.2、0.4 g/kg),再灌注24 h后进行神经学评分,测定脑梗死面积和脑含水量等短期药效评价。葡萄糖胺灌胃给药1 g/(kg.d)共24 d后,计算小鼠生存率以及进行爬杆测试评价肢体协调能力。结果 :葡萄糖胺(0.1～0.8 mmol/L)显著增加缺糖缺氧的HT22细胞的活性(P<0.05)。尾静脉注射葡萄糖胺(0.2、0.4 g/kg)能显著减小小鼠脑梗死面积,降低脑含水量并改善神经症状(P<0.05),连续灌胃给药后能显著增强小鼠肢体协调能力(P<0.05),但对动物死亡率无显著影响。结论:葡萄糖胺对脑缺血再灌注损伤具有保护作用。

The protective effect of glucosamine on cerebral ischemia-reperfusion injury

Objective: To observe the effect of glucosamine on the cerebral ischemia-reperfusion injury and provide the experimental evidence for its clinical applications.Methods: Oxygen-glucose deprivation(OGD) HT22 cell model was applied to observe the effect of glucosamine on the cell viability.Furthermore,mouse transient middle cerebral artery occlusion(tMCAO) model was employed,glucosamine was injected via tail vein before reperfusion,then assessed the short-term outcome: infarct area,the brain edema and neurological symptoms 24 h after ischemia-reperfusion.To observe the long-term outcome,the glucosamine was administrated intragastrically for 24 days,then survival rate and motor function were evaluated.Results: Glucosamine(0.1~0.8 mmol/L) reduced the cell death and LDH release induced by OGD treatment in HTT-22 cells.Glucosamine could significantly reduce the infarct area,ameliorate the brain edema and neurological symptoms at 24 h after ischemia/reperfusion in vivo.Additionally,in the long-term outcome study glucosamine markedly enhanced motor function but could not increased survival rate 24 days after ischemia-reperfusion injury.Conclusion: Glucosamine has neuroprotective effect on cerebral ischemia-reperfusion injury.