摘要
目的 探讨7,8-二羟基黄酮（D HF）对6-羟基多巴胺（6-O HD A）诱导PC12细胞损伤的保护作用及其机制。方法 将6-OHDA（25～200 Lmol/L）和PC12细胞混合后孵育24 h,观察6-O HD A的毒性作用;以D HF（1～25Lmol/L）预处理细胞1 h,再加入100 Lmol/L 6-O HDA继续培养24 h,观察D HF对6-O HD A诱导PC12细胞损伤的保护作用;25 Lmol/L D HF预处理前30 min加入10 n mol/L L Y294002,观察D HF的保护作用是否可被磷酸肌醇3激酶（PI3K）抑制剂所阻断。采用MTT法测定细胞存活率。结果 与对照组相比,50～200 Lmol/L 6-O HDA作用24 h可明显降低细胞存活率,其中100 Lmol/L 6-O HD A可导致半数细胞死亡。D HF预处理剂量依赖性抑制了6-OHDA诱导的细胞损伤,该作用部分被PI3K抑制剂所阻断。结论 DHF对6-OHDA诱导PC12细胞损伤具有明显的保护作用,该作用可能与PI3K信号通路有关。
Objective To investigate the protection of 7,8-dihydroxyflavone （DHF） on PC12 cell injury induced by 6 hydroxydopamine （6-OHDA） and its mechanism. Methods PC12 cells were incubated in different concentrations of 6-OHDA （25--200μmol/L） for 24 h to observe the toxic effect of 6-OHDA, the cells were then pretreated with DHF （1--25μmol/L） for lh, and exposed to 6-OHDA （100 μmol/L） for subsequent 24 h to observe the protection of DHF on PC12 cell injury induced by 6- OHDA. Finally, LY294002 （10 nmol/L, a PI3K inhibitor） was added before DHF （25 pmol/L） and 6-OHDA （100 μmol/L） treatment. The cell viability was measured by methyl thiazolyl tetrazolium （MTT） assay. Results Compared with the control group, 24 h treatment with 6-OHDA （50--200 μmol/L） markedly reduced the survival of PC12 cells, of which, the concentration of 100 μmol/L could result in the death up to 50%. DHF pretreatment dramatically suppressed the cell injury induced by 6-OHDA in a dose-dependent manner. The protective effect of DHF could be partially blocked by LY294002. Conclusion DHF shows an evident protection on PC12 cells against 6-OHDA-indueed injury, the effect is likely to be related with PI3K signal pathway.
出处
《青岛大学医学院学报》
CAS
2014年第1期4-6,共3页
Acta Academiae Medicinae Qingdao Universitatis
基金
国家自然科学基金资助项目(81070215)
山东省自然科学基金资助项目(ZR2010CM066)
山东省高等学校科研发展计划项目(J10LC16)
基础学院本科生创新项目
