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目的:探讨超负荷血糖对脑缺血再灌注损伤大鼠脑细胞凋亡及凋亡相关蛋白bax、bcl 2表达的影响。方法:用Wistar大鼠腹内注射链脲佐菌素,建立超负荷糖尿病大鼠模型,之后做大脑中动脉脑缺血再灌注模型。然后对大鼠进行脑梗死体积计算并且采用免疫组织化学方法检测超负荷血糖大鼠和正常大鼠脑缺血3h再灌注2 4hbax、bcl 2的表达,同时采用TUNEL法原位标记DNA片段,检测TUNEL阳性细胞的变化,并与假手术正常对照组比较。结果:超负荷血糖组梗死面积明显大于非超负荷血糖组;同时,前者bax的表达明显高于后者而bcl 2的表达则相反;糖尿病脑缺血再灌注损伤组TUNEL阳性细胞数明显高于非糖尿病脑缺血再灌注损伤和假手术对照组。结论:超负荷血糖加重了大鼠脑缺血再灌注损伤,超负荷血糖诱发的bax、bcl 2的表达异常促进了脑细胞的凋亡,可能是其加重脑缺血再灌注损伤的机制之一。
Objective: To investigate the effect of hyperglycemia on the apoptosis of brain cells and the expression of bax, bcl-2 in rats with cerebral ischemia-reperfusion injury. METHODS: Streptozotocin (STZ) was intraperitoneally injected into Wistar rats to establish a model of overloaded diabetic rats and then a middle cerebral artery occlusion (MCAO) model of cerebral ischemia reperfusion. Then the cerebral infarction volume was calculated and the expression of 24hbax and bcl2 was detected by immunohistochemical method in 3h after cerebral ischemia in overload and normal rats. DNA fragments were detected by TUNEL in situ. TUNEL positive cells were observed and compared with sham-operated normal control group. Results: The area of infarction in hyperglycemia group was significantly larger than that in non-hyperglycemia group. Meanwhile, the expression of bax in the former was significantly higher than that in the latter while the expression of bcl 2 was opposite. The number of TUNEL positive cells in diabetic cerebral ischemia-reperfusion group was significantly higher than that in non- Non-diabetic cerebral ischemia-reperfusion injury and sham operation control group. Conclusions: Excessive blood glucose aggravates cerebral ischemia-reperfusion injury in rats. Abnormal expression of bax and bcl2 induced by hyperglycemia promotes the apoptosis of brain cells, which may be one of the mechanisms that aggravate cerebral ischemia-reperfusion injury .