过表达脑红蛋白对SH-SY5Y细胞损伤的神经保护作用及其机制  被引量:2

Neuroprotection of overexpression of neuroglobin gene on injury of SH-SY5Y cells and relevant mechanism

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作  者:张雄[1] 孙洁芸[1,2] 高敏娜[2] 李昱[1,2] 

机构地区:[1]重庆医科大学神经科学研究中心,重庆400016 [2]重庆医科大学病理教研室,重庆400016

出  处:《中国生物制品学杂志》2013年第12期1768-1771,共4页Chinese Journal of Biologicals

基  金:国家自然科学基金资助项目(81100948)

摘  要:目的探讨过表达脑红蛋白(neuroglobin,NGB)对水溶性β-淀粉样蛋白片段1-42(beta-amyloid1-42,Aβ1-42)诱导的神经母细胞瘤SH-SY5Y细胞损伤的神经保护作用及其机制。方法将质粒pEGFP-NGB转染经Aβ1-42诱导损伤的SH-SY5Y细胞,MTT法检测NGB对损伤细胞存活率的影响;JC-1染色法检测NGB对损伤细胞线粒体膜电位的影响;免疫细胞化学法及Western blot法分别检测损伤细胞中细胞色素C(cytochrome C,cytoC)和caspase-3、caspase-9的表达水平。结果过表达NGB可明显提高Aβ1-42诱导损伤的SH-SY5Y细胞的存活率(P<0.05),抑制损伤细胞线粒体膜电位的降低(P<0.01),使损伤细胞内cytoC和caspase-3、caspase-9蛋白的表达水平均明显降低(P<0.05)。结论 NGB可通过抑制与细胞凋亡密切相关的cytoC、caspase-3和caspase-9等蛋白的表达而发挥其神经保护作用。本实验为阿尔茨海默病(Alzheimer disease,AD)的治疗提供了实验依据。Objective To investigate the neuroprotective effect of overexpression of neuroglobin (NGB) gene on the injury of neurocytoma SH-SY5Y cells induced by soluble beta-amyloid 1-42 (A13L42) as well as the relevant mechanism. Methods SH-SY5Y cells pretreated with Aβ1-42 were transfected with plasmid pEGFP-NGB, then determined for smwival rate by MTI" assay, for membrane potential of mitochondrial by JC-1 staining, and for expression levels of eytochrome C(cytoC) as well as cysteine-containing caspase-3 and -9 by immunocytochemical assay. Results NGB overexpression increased the smwival rate of Stt-SY5Y cells treated with Aβ1-42 (P 〈 0. 05), while inhibited the decrease of membrane potenlial of mitochondrial (P 〈 0. 01 ) as well as the expression levels of cytoC, caspase-3 and -9 (P 〈 0. 05). Conclusion NGB play a neuroprotective gave play to its neuroprotection to SH-SY5Y cells through inhibiting the expressions of eytoC, caspase-3 and -9, which provided an experimental basis for treatment of Alzheimer disease (AD).

关 键 词:脑红蛋白 SH-SY5Y细胞 细胞损伤 β-淀粉样蛋白片段 

分 类 号:Q256[生物学—细胞生物学] R739.4[医药卫生—肿瘤]

 

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