MCI-186对Aβ_(25-35)诱导PC12细胞氧化损伤的神经保护作用  被引量:5

Neuroprotective effects of MCI-186 on PC12 cells induced by Aβ_(25-35)

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作  者:于明[1] 张晓林[1] 冷闻辉[1] 李淑娟[1] 陈慧娟[1] 

机构地区:[1]江苏大学附属医院神经内科,镇江212002

出  处:《江苏医药》2009年第11期1317-1320,共4页Jiangsu Medical Journal

基  金:江苏大学附属医院引进人才课题(jdfyRC2008003)

摘  要:目的探讨MCI-186(edaravone)对阿尔茨海默病(AD)细胞损伤的保护作用。方法利用淀粉样β蛋白25-35(Aβ25-35)诱导PC12细胞制备成AD细胞模型;采用MTT法确定Aβ25-35抑制PC12细胞生长的半数抑制浓度(IC50)和MCI-186对AD细胞保护作用最强时的浓度;利用邻菲罗啉化学发光法测定羟自由基(.OH)含量,确定MCI-186清除.OH最强作用时的浓度。结果Aβ25-35诱导PC12细胞的IC50是29.76μmol/L,此浓度的Aβ25-35对PC12细胞生长的最大抑制率发生在36 h;30μmol/L Aβ25-35诱导PC12细胞36 h可以制成理想的AD细胞模型。20μmol/L MCI-186清除.OH作用最强,即对AD细胞的保护作用最强。结论MCI-186可以通过清除Aβ25-35产生的.OH,在AD中发挥其神经细胞保护作用。Objective To evaluate the protective effects of MCI-186 (edaravone) on the heochromocytoma-derived cell line (PC12 cells) induced by amyloid beta protein (Aβ25-35). Methods The cell model of Alzheimer's disease (AD) was set up by means of inducing PC12 cells with Aβ25-35. Survival rate of PC12 cells was detected by MTT assay, and scavenging effect of ^·OH was determined with CuSO4-PHEN-VitC-H2O2 biochemiluminescence system. Results The median inhibitory concentration (IC50) of Aβ25-35 inhibiting PC12 cells growth was 29.76 μmol/L, at which the maxium inhibitory rate of PC12 cells growth was found at 36 h.Aβ25-35 at concentration of 30 μmol/L inducing PC12 cells for 36 h could develop an ideal AD cell model. MCI-186 in a concentration of 20 μmol/L had the strangest effect for quenching ^·OH generated by Aβ25-35 and protecting the AD cells. Conclusion MCI-186, a novel free radical scovenger, has an neuroprotective effect, which may be through inhibiting ^·OH produced by Aβ25-35.

关 键 词:MCI-186 淀粉样口蛋白 PC12细胞 自由基 

分 类 号:R742[医药卫生—神经病学与精神病学]

 

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