厚朴酚对抗6-OHDA诱导PC12细胞损伤的作用机理研究

Mechanisms of magnolol against 6-OHDA-induced PC12 cell trauma

目的:探讨厚朴酚对6-羟基多巴胺(6-OHDA)诱导PC12细胞损伤的保护作用可能机制。方法:将厚朴酚或6-OH-DA加入培养的PC12细胞中。四甲基偶氮唑蓝法(MTT法)检测细胞活力,用荧光分光计法测定细胞损伤过程中活性氧、半胱氨酸蛋白酶3的含量变化。结果:在加入100μmol/L6-OHDA时PC12细胞活性显著下降,厚朴酚(0.1～10μmol/L)预处理1h可明显抑制6-OHDA导致的PC12细胞活性下降,ROS含量水平的上升以及caspase-3的活性上升。结论:厚朴酚对6-OHDA诱导的PC12细胞损伤有一定的保护作用,其作用机制涉及到抑制细胞内ROS的产生和Caspase-3的激活。

AIM ： To investigate the possible mechanism of magnolol on the damage of PC12 cell induced by the addition of 6-OHDA placed in an incubator for 24 h with rat＇ s pheochromocytoma cell of adrenal medulla in the absence and presence of magnolol. METHODS： Cell viability was measured by MTF method. Reactive oxygen species （ROS） and aspartate-specific cysteine proteases-3 （Caspase-3） concentration （s） were assayed by fluorescence spectrophotometer. RESULTS： Cell activity declined sharply by the addition of 6-OHDA at concentration of 100 μmol/L, the pre-treatment of magnolol（0.1 - 10 μmol/L） could significantly increase the PCI2 cell activity and prevent the increased ROS and caspase-3. CONCLUSION： Magnolol may protect the cell trauma induced by 6-OHDA, and the mechanism is related to inhibiting the 6-OHDA-induced elevation in intracellular ROS levels and reducing the caspase-3 activity.