新生大鼠缺氧、缺血合并高、低血糖的脑细胞凋亡研究

Morphological study of neuronal apoptosis in neonatal rat models with both hypoxic ischemia associated with hyper and hypoglycemia

目的应用显微镜观察及原位末端标记技术,对新生大鼠缺氧、缺血(HI)合并高、低血糖模型进行脑细胞凋亡形态学研究。方法7日龄SD新生大鼠通过不同的模型制备方法,分为8组:正常对照组、假手术组、HI组、HI前轻度高血糖组、HI前重度高血糖组、HI前低血糖组、HI后轻度高血糖组及HI后重度高血糖组。在对新生大鼠HI合并高、低血糖模型进行脑病理研究的同时,运用原位末端标记技术进一步对其进行脑细胞凋亡形态学研究,观察不同血糖浓度对脑细胞凋亡造成的影响。结果HI前重度高血糖组大鼠的脑凋亡细胞数明显减少,而HI前低血糖组大鼠的脑凋亡细胞数明显增加。提示HI前重度高血糖可显著减轻HI后脑细胞凋亡,HI前低血糖则可进一步加剧HI后脑细胞凋亡。结论HI前重度高血糖减轻HI后脑细胞凋亡的机制可能与其补充了一定量的葡萄糖,使能源物质不至匮乏,因而避免或减轻脑HI损伤加剧及脑细胞凋亡有关。

Objective Morphological study of neuronal apoptosis was undertaken in neonatal rat models with both hypoxic ischemia （HI）, associated with hyper and hypoglycemia. Methods Apoptotic brain cells with either HE dying or ISEL labeling were counted under microscope. 7-day-old SD rats were randomly divided into 8 groups including normal control group, sham-operation group, HI group, groups with mild hyperglycemia before or after HI, group with severe hyperglycemia before or after HI, and group with hypoglycemia before HI, respectively. Results Apoptotic cells decreased obviously in the group with severe hyperglycemia before HI, while there was a significant increase in the group with hypoglycemia before HI. Hence it was suggested that the former could decrease and the latter could enhance the neuronal apoptosis after HI. Conclusion Adequate glucose as energy source can protect brain tissue against neuronal apoptosis following HI. （Shanghai Med J, 2005,28：786- 789）