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目的 探讨肉苁蓉总苷(GCs)对脑缺血再灌注所致清醒小鼠海马CA_1区脑组织损伤的保护作用。方法 结扎小鼠右侧颈总动脉建立脑缺血及脑缺血再灌注模型,动态观察GCs对脑缺血3小时再灌注24及48小时两个时点脑梗死范围百分比、脑缺血3小时再灌注24小时海马CA_1区脑组织病理变化及脑细胞凋亡情况的影响。结果脑缺血及脑缺血再灌注后脑梗死范围百分比明显增加;海马CA_1区脑细胞密度降低,细胞皱缩明显,胞浆染色较深,核染色质凝聚,凋亡神经细胞明显增多;与缺血组相比,缺血再灌注组损伤加重。GCs可促进上述各项指标的恢复,显著降低脑梗死范围百分比,减轻脑组织病理损伤,抑制脑细胞凋亡。结论GCs对脑缺血再灌注小鼠脑组织具有保护作用,其机制可能与抗氧化及抗脑细胞凋亡作用有关。
Objective To investigate the protective effects of glycosides of cistanche (GCs) on brain tissue damage in hippocampal CA_1 of awake mice induced by cerebral ischemia-reperfusion. METHODS: The right common carotid artery was ligated to establish a model of cerebral ischemia and cerebral ischemia-reperfusion. The percentage of cerebral infarct scope and cerebral ischemia at 2 hours after 24 hours and 48 hours of cerebral ischemia at 3 hours after cerebral ischemia were dynamically observed. The pathological changes of hippocampal CA_1 region and the effect of brain cell apoptosis after 24 hours of reperfusion. Results The percentage of cerebral infarction was significantly increased after cerebral ischemia and cerebral ischemia-reperfusion. The brain cell density of hippocampal CA1 decreased, the cell shrinkage was obvious, the cytoplasm stained deeper, the chromatin condensed, and the number of apoptotic nerve cells increased. Compared with the blood group, the ischemia-reperfusion injury was aggravated. GCs can promote the recovery of the above indicators, significantly reduce the percentage of cerebral infarction, reduce brain tissue pathological damage, inhibit brain cell apoptosis. Conclusion GCs has a protective effect on brain tissue of cerebral ischemia-reperfusion mice. Its mechanism may be related to its anti-oxidation and anti-apoptosis effects on brain cells.