木豆素A对皮质酮诱导的PC12细胞损伤的保护作用

Neuroprotective effect of longistyline A against corticosteroneinduced neurotoxicity in PC12 cells

利用皮质酮诱导PC12细胞损伤模型,研究木豆素A对皮质酮诱导的PC12细胞的保护作用并探讨相应的保护途径。采用100μmol.L1皮质酮与PC12细胞作用48 h,诱导PC12细胞损伤,然后与不同浓度的木豆素A孵育24 h。检测细胞存活率、LDH渗漏量、细胞内Ca2+浓度及caspase-3活性。结果显示,PC12细胞与皮质酮孵育48 h后细胞存活率明显降低,而LDH漏出量、细胞内Ca2+浓度及caspase-3活性均显著升高;木豆素A(4.0、8.0及16.0μmol.L1)具有改善作用,但量效关系不明显。研究表明,木豆素A对皮质酮诱导的PC12细胞损伤具有明显的保护作用,其保护作用可能是通过降低Ca2+浓度及caspase-3活性来实现的。

This study is to investigate the protective effect of longistyline A against corticosterone-induced neurotoxicity in PC12 cells.While PC12 cells were exposed to 100 μmol-L-1 corticosterone for 48 h,cell survival rate was reduced and lactate dehydrogenase（LDH） release increased.In parallel,corticosterone caused significant elevations of DNA fragmentation,i and caspase-3 activity.However,when the PC12 cells were incubated with longistyline A（4.0,8.0 and 16.0 μmol-L-1） in the presence of 100 μmol-L-1 corticosterone for 48 h,the effects were evidently alleviated,but dose-dependent manner was not obvious.In summary,longistyline A could generate a neuroprotective effect against corticosterone-induced neurotoxicity in PC12 cells possibly by decreasing i and caspase-3 activity.