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本文旨在探讨重组人红细胞生成素(recombinant human erythropoietin, rhEPO)是否通过抑制甘油醛三磷酸脱氢酶(glyc-eraldehyde-3-phosphate dehydrogenase, GAPDH)核内过表达减少脑缺血再灌注大鼠神经元凋亡。大脑中动脉栓塞法制作脑缺血再灌注大鼠模型。48只Sprague-Dawley大鼠随机分为假手术组、生理盐水对照组和EPO处理组。TTC染色、尼氏染色及Hoechst-33258免疫荧光分别观察EPO对脑组织缺血和缺血半影区神经元凋亡的影响;Hoechst-33258和GAPDH免疫荧光双染观察EPO对GAPDH核内过表达的影响。结果显示,与生理盐水对照组相比,再灌注同时开始给予rhEPO (3 000 U/kg,3次/日,腹腔注射)显著抑制缺血再灌注引起的神经元GAPDH核内过表达,同时显著减少半影区神经元凋亡数目,减轻缺血性脑损伤。以上结果提示,rhEPO可能通过抑制GAPDH核内过表达减少脑缺血再灌注大鼠半影区神经元凋亡,为探讨EPO的神经保护机制提供了实验证据。
This study aimed to investigate whether recombinant human erythropoietin (rhEPO) can reduce cerebral ischemia-reperfusion injury by inhibiting the overexpression of glycated ehtyl-3-phosphate dehydrogenase (GAPDH) Neuronal apoptosis. Cerebral ischemia - reperfusion rat model by middle cerebral artery occlusion. 48 Sprague-Dawley rats were randomly divided into sham operation group, saline control group and EPO treatment group. TTC staining, Nissl staining and Hoechst-33258 immunofluorescence were used to observe the effects of EPO on neuronal apoptosis in ischemic penumbra and ischemic area of the brain respectively. Double immunofluorescence staining with Hoechst-33258 and GAPDH was used to observe the effect of EPO on nuclear over-expression in GAPDH Impact. The results showed that rhEPO (3 000 U / kg, 3 times / day, intraperitoneal injection) significantly inhibited the nuclear over-expression of GAPDH induced by ischemia-reperfusion in reperfusion compared with saline control group, Reduce the number of neuronal apoptosis in the penumbra, reduce ischemic brain damage. The above results suggest that rhEPO may provide experimental evidence for exploring the neuroprotective mechanism of EPO by inhibiting the overexpression of GAPDH nucleus and decreasing the neuronal apoptosis in the penumbra of cerebral ischemia-reperfusion rats.