非糖尿病性脑梗死与急性期高血糖的相关性及机制

The correlation between non-diabetic cerebral infarction and acute hyperglycemia and its mechanism

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 explore the correlation between non- diabetic cerebral infarction and acute hyperglycemia and its possible mechanism. Methods In this experiment, twenty- four SD rats were randomly divided into three groups, normoglycemia group（NG）, two hyperglycemia groups（HG1 and HG2）.Rats were rendered acute hyperglycemia during occluded the middle cerebral artery（MCAO）.To assess the correlation between non- diabetic cerebral infarction and acute hyperglycemia, the rats were observed for neurological functional impairment scoring and cerebral infarct volumes at 24 h after cerebral infarction. At the same time, the proliferation capacity of neural stem cell in ischemic ipsilateral dentate gyrus was observed.Results The levels of blood glucose of NG group was 4.0-5.0 mmol/L,and HG1 and HG2 groups were markedly up to the target blood glucose concentrations of 10.0 mmol/L and 20.0 mmol/L, respectively（P0.01）. 24 h after MCAO, cerebral infarct volumes of HG2 group were obviously more larger than NG group and HG1 group（P0.05）, which suffered from more severe neurological impairment（P0.05）. However,there were no significant difference in cerebral infarct volumes and neurological deficits between HG1 group and NG group（P0.05）. The proliferation capacity of neural stem cells detection results were consistent with that of neurological deficits and cerebral infarct volumes. Conclusion Mild acute hyperglycemia（10.0mmol/L） may protect the neural stem cells against the infarction cerebral injury. Severe hyperglycemia（20mmol/L） obviously deteriorated infarct brain injury, which may be associated with impaired proliferation capacity of neural stem cells.