摘要
目的：探讨三七皂苷R1对Aβ1-42诱导SH-SY5Y细胞凋亡的保护机制。方法：MIT法检测细胞存活率；PI／Annexin V双染流式细胞术分析细胞凋亡率；Westernblot法检测细胞中Bax，Bcl-2的表达；ELISA法检测easpase-3，caspase-8及caspase-9的酶活性。结果：6．25，12．5，25，50，100nmol·L^-1的三七皂苷R1对Aβ1-42诱导的SH-SY5Y细胞凋亡均有一定保护作用，并呈剂量依赖关系；PI／Annexin V双染流式细胞术检测结果表明Aβ1-42可诱导SH-SYSY细胞发生凋亡，6．25～100nmol·L^-1的三七皂苷R1可显著降低细胞凋亡率。Westernblot结果显示，6．25～100nmol·L^-1的三七皂苷R1可下调Bax表达，上调Bcl-2表达；ELISA分析显示不同剂量的三七皂苷R1可抑制Aβ1-42诱导的SH-SY5Y细胞caspase-3和caspase-9的激活，但对caspase-8的激活没有影响。结论：三七皂苷R1通过抑制线粒体相关的凋亡通路激活，减少Aβ1-42诱导的SH-SYSY细胞凋亡。
Objective： To investigate the effects and underlying mechanism of notoginsenoside R1 on amyloid-β（1-42） （ Aβ1-42 ） in- duced mitochondrial apoptotic death in SH-SY5Y cells. Method： Cell viability was assayed by MTT, apoptotic rates were analyzed with PI/Annexin V flow cytometry, Bax and Bcl-2 expression were detected with Western blotting, enzymatic activity of caspase-3, caspase-8 and caspase-9 were measured by ELISA assay. Result： The 6. 25-100 nmol· L^-1 of notoginsenoside R1 attenuate Aβ1-42 in- duced apoptotic death of SH-SY5Y in dose dependent manner. The ratio of Bcl-2/Bax was elevated in SH-SY5Y with notoginsenoside R1 treatment. Caspase-3 and caspase-9 were activated with notoginsenoside R1 treatment while caspase-8 was not affected. Conclu- sion： Notoginsenoside R1 could protect SH-SYSY cells from Aβ1-42 induced apoptosis via mitochondria related apoptotic pathway.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2015年第2期303-307,共5页
China Journal of Chinese Materia Medica
基金
国家"重大新药创制"科技重大专项(2012ZX09103-201)
