二氢石蒜碱对过氧化氢损伤的PC12细胞的保护作用

目的:探讨二氢石蒜碱(DL)对H2O2诱导的PC12细胞氧化损伤的影响及其可能机制。方法:用H2O2(200μmol.L-1)处理PC12细胞建立氧化应激模型,并加入二氢石蒜碱预处理作为保护。噻唑蓝(MTT)法和乳酸脱氢酶(LDH)检测细胞存活率和细胞损伤程度,利用荧光探针DCFH-DA和JC-1分别检测细胞内活性氧(ROS)和线粒体膜电位。结果:H2O2作用于PC12细胞后,细胞存活率下降,LDH活性和ROS含量增高,线粒体膜电位降低,与正常对照组比较具有显著性差异(P<0.01);10-7～10-5mol.L-1DL预处理后,细胞存活率提高,LDH和ROS变低,线粒体膜电位回升,且在一定范围呈剂量依赖性。结论:DL对H2O2诱导PC12细胞氧化损伤具有保护作用,其作用机制可能与减少ROS产生和稳定线粒体膜电位有关。

Protective effect of dihydrolycorine on H2O2-induced oxidative stress damage in PC12 cells

Objective: To investigate the protective effect of dihydrolycorine(DL) on H2O2-induced oxidative stress damage in PC12 cells.Methods: Oxidative stress damage of PC12 cells was induced by H2O2 at 200 μmol·L-1.The survival rate and damage degree were determined by MTT reduction assay and lactate dehydrogenase(LDH) release.Intracellular reactive oxygen species(ROS) generation and the changes in mitochondrial membrane potential were detected by fluorescent probe DCFH-DA and JC-1,respectively.Results: Compared with the normal control,H2O2 reduced the cell viability and depressed mitochondrial membrane potential,whereas increased LDH release and ROS production.Pretreatment with DL(10-7~10-5 mol·L-1) attenuated viability reduction,depression of mitochondrial membrane potential,LDH release and ROS generation induced by H2O2.Conclusion: DL protects PC12 cells against H2O2-induced oxidative stress damage and its mechanism may be related to ROS decrease and stability of mitochondrial membrane potential.