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【目的】探讨谷氨酸受体阻滞剂(GYKI52466)对缺氧缺血性脑病(hypoxic-ischemic encephalopathy,HIE)新生大鼠脑细胞凋亡的抑制作用。【方法】体内实验:将新生大鼠随机分为空白对照组(N组)、缺氧缺血性脑损伤组(H组)与GYKI52466干预组(G组)。造模后给药,观察各组大鼠的神经行为学异常及超微结构变化。体外实验:将各组新生大鼠的脑细胞制成单细胞悬液,培养4d后,N组给予正常环境培养,H组给予缺氧缺糖环境,G组给予缺氧缺糖环境后添加GYKI52466培养,6h后比较各组细胞生长状态,采用流式细胞仪进行脑细胞凋亡分析。【结果】体内实验:神经行为学观察,G组与H组相比,异常神经行为学有所改善;电镜下观察,H组神经元细胞核结构破坏,核膜破裂、核仁轻度皱缩,而G组结构趋向完整。体外实验:与模型组相比,G组的细胞凋亡数明显减少,数值差异有高度统计学意义(P<0.001)。【结论】谷氨酸受体阻滞剂GYKI25466有效的减轻新生大鼠缺氧缺血性脑病时异常的神经行为学表现和病理学改变,抑制神经细胞细胞凋亡,证实GYKI25466具有一定的神经保护作用。
【Aim】 To investigate the inhibitory effect of glutamate blockade (GYKI52466) on the apoptosis of neonatal rat brain during hypoxic-ischemic encephalopathy (HIE). 【Methods】 In vivo experiments: Newborn rats were randomly divided into blank control group (N group), hypoxic-ischemic brain injury group (H group) and GYKI52466 intervention group (G group). After administration, the neurobehavioral abnormalities and ultrastructural changes of the rats in each group were observed. In vitro experiments: The brain cells of neonatal rats in each group were made into single cell suspension. After cultured for 4 days, N group was given normal environment culture, H group was given hypoxic-hypoglycemic environment, G group was given hypoxic-hypoglycemic environment and GYKI52466 After 6 hours, the cell growth status of each group was compared, and the apoptosis of brain cells was analyzed by flow cytometry. 【Results】 In vivo, neurobehavioral observation showed that abnormal neurobehavioral changes were observed in group G compared with those in group H. Under electron microscope, the nuclear structure of neurons in H group was disrupted, ruptured nuclear membrane, slight rupture of nucleolus, The G group tends to be complete. In vitro experiments: compared with the model group, the number of apoptotic cells in G group decreased significantly, the difference was highly statistically significant (P <0.001). 【Conclusion】 Glutamate receptor blocker GYKI25466 can effectively alleviate the abnormal neurobehavioral changes and pathological changes in neonatal rats with hypoxic-ischemic encephalopathy and inhibit the apoptosis of neuronal cells, confirming that GYKI25466 has certain neuroprotective effect.