摘要
目的研究依达拉奉(MCI-186)对阿尔茨海默病(AD)细胞损伤的保护作用及其机制。方法将人神经母细胞瘤SH-SY5Y细胞分为五组:空白对照组、溶剂对照组、β淀粉样肽(Aβ)组、Aβ+溶剂对照组和Aβ+药物处理组。用Aβ25-35处理SH-SY5Y细胞,建立AD细胞模型。采用DAPI荧光染色法计数凋亡细胞,Western blot法检测磷酸化的p38丝裂原活化蛋白激酶(p-p38MAPK)表达。结果 Aβ25-35引起时间和剂量依赖性的SH-SY5Y细胞凋亡,并使p-p38MAPK表达增加(P<0.05)。MCI-186与p38MAPK抑制剂SB239063均抑制Aβ25-35诱导的SH-SY5Y细胞凋亡及p-p38MAPK表达(P<0.05)。结论 MCI-186通过抑制p38MAPK磷酸化,对Aβ25-35诱导的SH-SY5Y细胞凋亡起到保护作用。
Objective To investigate the protective effect and mechanism of edaravone（MCI-186） on cell injury of Alzheimer′s disease（AD）. Methods The human neuroblastoma SH-SY5Y cells were divided into control group,solvent group,amyloid-β peptide（Aβ） group,Aβ＋solvent group and Aβ＋drug group. The SH-SY5Y cells were treated with Aβ25-35 to establish AD model.The apoptic cells were counted by DAPI assay,and the expression of phosphorylated p38 mitogen-activated protein kinases（p-p38MAPK） was detected by Western blot. Results Aβ25-35 induced the apoptosis of SH-SY5Y cells in the time-and dose-dependent manner and up-regulated the expression of p-p38MAPK（P0.05）. Both MCI-186 and p38MAPK inhibitor SB239063 inhibited the apoptosis of SH-SY5Y cells and the expression of p-p38MAPK induced by Aβ25-35（P0.05）. Conclusion MCI-186 may protect the SH-SY5Y cells from Aβ-induced injury through inhibiting the phosphorylation of p38MAPK.
出处
《江苏医药》
CAS
CSCD
北大核心
2012年第1期27-30,共4页
Jiangsu Medical Journal
