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目的探讨GAPDH从胞浆移位入核内在EPO减轻脑缺血大鼠神经损伤机制中的作用。方法 36只SD大鼠随机分为假手术组、生理盐水对照组和EPO处理组。制作大脑中动脉栓塞脑缺血再灌注大鼠模型,用TTC染色法观察EPO对脑组织损伤情况的影响;用Hoechest-33258和GAPDH免疫组化双染观察EPO对GAPDH核内过表达的影响;用Hoechest-33258免疫荧光观察EPO对缺血半影区神经元凋亡的影响。结果大鼠脑缺血2 h再灌注24 h及48 h,与生理盐水对照组相比,缺血同时开始给予rhEPO(3000 U/kg,3次/d,腹腔注射)显著减轻缺血脑组织损伤范围、抑制缺血再灌注引起的GAPDH从神经元胞浆移位入核内引起的神经元凋亡。结论 GAPDH移位入核内,在rhEPO减轻脑缺血再灌注引起的神经损伤的机制中起重要作用。
Objective To investigate the effect of GAPDH translocation from the cytoplasm to the nucleus in the mechanism of neuroprotection induced by EPO in rats with cerebral ischemia. Methods Thirty - six SD rats were randomly divided into sham operation group, saline control group and EPO treatment group. The model of middle cerebral artery occlusion with cerebral ischemia-reperfusion was established. The effect of EPO on the damage of brain tissue was observed by TTC staining. The effect of EPO on the overexpression of GAPDH was observed by immunohistochemical double staining with Hoechest-33258 and GAPDH. The effect of EPO on neuronal apoptosis in the penumbra was observed with Hoechest-33258 immunofluorescence. Results Compared with the saline control group, rhEPO (3000 U / kg, 3 times / d, intraperitoneal injection) at the same time of ischemia was significantly reduced in ischemic brain tissue at 24 h and 48 h after cerebral ischemia 2 h reperfusion The extent of injury inhibits neuronal apoptosis induced by ischemia-reperfusion-induced GAPDH translocation from neuronal cytoplasm into the nucleus. Conclusion GAPDH translocates into the nucleus and plays an important role in the mechanism of rhEPO in ameliorating the mechanism of nerve injury induced by cerebral ischemia-reperfusion.