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目的:探讨星形胶质细胞在高血糖脑缺血再灌注损伤中的变化规律。方法:采用链脲佐菌素(STZ)诱导Ⅰ型糖尿病高血糖大鼠模型,通过双侧颈总动脉夹闭联合股动脉放血法建立全脑缺血再灌注模型,应用组织学、免疫荧光、组织化学及Western Blot方法,对比观察糖尿病高血糖脑缺血再灌注组(简称糖尿病组)与正常血糖脑缺血再灌注组(简称正常血糖组)在脑缺血15 min、再灌注1 h和6 h大脑额叶皮质区神经元、星形胶质细胞组织学变化及GFAP的表达。结果:正常血糖组再灌注1 h脑组织出现轻度水肿;再灌注6 h脑水肿加重,出现神经元固缩;再灌注1 h,糖尿病组病变与正常血糖组基本相同,再灌注6 h脑水肿加重,固缩神经元进一步增加。再灌注1 h和6 h,糖尿病组Nissl体平均光密度值明显低于正常血糖组(P<0.05)。脑组织GFAP免疫荧光检查可见,再灌注6 h正常血糖组GFAP免疫阳性细胞明显增加。糖尿病组再灌注1 h和6 h,出现GFAP阳性星形胶质细胞数目增加(P<0.05),胞体显著增大,突起增长、增粗。Western Blot结果可见,糖尿病组GFAP的表达明显高于正常血糖组。结论:糖尿病高血糖脑缺血再灌注能够加重神经元损伤,星形胶质细胞出现更明显的数量增加和GFAP表达。
Objective: To investigate the changes of astrocytes in hyperglycemic ischemia-reperfusion injury. Methods: A rat model of type 1 diabetes mellitus with hyperglycemia was induced by streptozotocin (STZ). The model of global cerebral ischemia-reperfusion was established by bilateral common carotid artery occlusion and femoral artery bleeding. The histological, immunofluorescence, Histochemistry and Western Blot method were used to observe the changes of cerebral ischemia-reperfusion group (referred to as diabetic group) and normal blood-glucose-ischemia-reperfusion group (normal blood glucose group) at 15 min of cerebral ischemia and 1 h of reperfusion Histological changes of neurons and astrocytes in 6 h brain frontal cortex and GFAP expression. Results: In the normal blood glucose group, mild edema appeared in the brain tissue at 1 h after reperfusion. Cerebral edema was aggravated at 6 h after reperfusion, and pyknosis of neurons was observed at 1 h after reperfusion. The pathological changes in diabetic group were basically the same as those in normal blood glucose group, Edema aggravated, further increase in pyknotic neurons. At 1 h and 6 h after reperfusion, the average optical density of Nissl body in diabetic group was significantly lower than that in normal glucose group (P <0.05). GFAP immunofluorescence showed that GFAP immunoreactive cells in normal blood glucose group increased significantly at 6 h after reperfusion. At 1 and 6 h after reperfusion, the number of GFAP positive astrocytes in diabetic group increased (P <0.05), the number of somatic cells increased significantly, and the number of protrusions increased and increased. Western Blot results showed that the expression of GFAP in diabetic group was significantly higher than that of normal blood glucose group. CONCLUSION: Cerebral ischemia-reperfusion in diabetic hyperglycemia can exacerbate neuronal damage, with a marked increase in the number of astrocytes and GFAP expression.