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目的探讨非糖尿病性脑梗死与急性期高血糖的相关性及机制。方法 24只SD大鼠随机分为正常血糖组(NG)、高血糖1组和2组(HG1和HG2),脑缺血(middle cerebral artery occlusion,MCAO)期间诱导急性期高血糖。MCAO后24h观察神经功能缺损评分和脑梗死灶以了解非糖尿病性脑梗死与急性期高血糖相关性,并观察缺血同侧齿状回神经干细胞增殖能力。结果 NG组、HG1组和HG2组血糖分别达约4.0~5.0 mmol/L、10.0 mmol/L和20.0 mmol/L目标值。HG2组神经功能缺损评分及脑梗死灶均比NG组、HG1组大,差异具统计学意义(P<0.05);HG1组与NG组间差异均无统计学意义(P>0.05)。神经干细胞增殖能力改变与神经功能缺损评分及脑梗死灶检测结果一致。结论轻度急性期高血糖(10.0 mmol/L)可能通过保护受损的神经干细胞而不加重梗死性脑损伤,重度急性期高血糖(20.0mmol/L)则可能通过恶化神经干细胞增殖能力加重梗死性脑损伤。
Objective To investigate the correlation between non-diabetic cerebral infarction and acute hyperglycemia and its mechanism. Methods Twenty-four SD rats were randomly divided into normal glucose group (NG), hyperglycemia group 1 and 2 (HG1 and HG2), and acute hyperglycemia during middle cerebral artery occlusion (MCAO). Neurological deficit scores and cerebral infarction were observed 24h after MCAO to find out the correlation between non-diabetic cerebral infarction and acute hyperglycemia and to observe the proliferation of ipsilateral dentate gyrus neural stem cells. Results The blood glucose of NG group, HG1 group and HG2 group reached about 4.0-5.0 mmol / L, 10.0 mmol / L and 20.0 mmol / L respectively. The scores of neurological deficit and cerebral infarction in HG2 group were higher than those in NG group and HG1 group (P <0.05). There was no significant difference between HG1 group and NG group (P> 0.05). Changes in neural stem cell proliferation and neurological deficit scores and cerebral infarction consistent with the test results. Conclusions Mild acute hyperglycemia (10.0 mmol / L) may protect the damaged neural stem cells without aggravating infarct brain injury. Severe acute hyperglycemia (20.0 mmol / L) may aggravate the infarction by worsening the proliferation of neural stem cells Brain damage.