【摘要】 目的:研究PC12细胞缺糖损伤的分子生物学特征。方法:建立细胞缺糖模型,电镜观测PC12细胞形态;SOD法检测超氧化物歧化酶活性;流式细胞仪检测细胞凋亡率;RT-PCR测定bcl-2、bcl-xl基因表达。结果:缺糖细胞有凋亡现象发生;细胞缺糖24 h后,培养液内的SOD和细胞内的SOD活力明显降低;bcl-2、bcl-xl基因在6~16 h表达上调,此后表达下调。结论:缺糖损伤的PC12细胞既有形态的变化也有功能的变化,细胞膜受到自由基的攻击,细胞抗氧化能力下降,细胞同时伴随着凋亡和坏死两种死亡方式,bcl-2、bcl-xl基因的表达具有一定的时序和范围特点。更多还原

【Abstract】 Objective:To probe into the pathological mechanism of the injury induced by glucose deprivation(an insult relevant to the brain ischemia) in PC12 cell line,providing a basis for studying the mechaism for post-eschemia neuron damage.Methods: Electron microscopy,SOD measurement,Flow Cytometry and RT-PCR were used.Results: The apoptosis and necrosis were observed in the treated PC12 cells,with significant decrease of SOD values.Bcl2 and bcl-xl RNA expression upregulated from 6 to 16 hours after glucose deprivation treatment and declined gradually since then.Conclusion: The PC12 cells deprived of glucose have the morphological and functional alterations including apoptosis and necrosis.更多还原