论文部分内容阅读
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。
AIM: To investigate the effects of dihydropalcinate (DL) on H2O2-induced oxidative damage in PC12 cells and its possible mechanism. Methods: PC12 cells were treated with H2O2 (200μmol.L-1) to establish an oxidative stress model, and dihydrotestination pretreatment was used as protection. MTT and LDH were used to detect cell viability and cell injury. Fluorescent probes DCFH-DA and JC-1 were used to detect intracellular reactive oxygen species (ROS) and mitochondrial membrane potential. Results: After H2O2 treatment, the cell viability decreased, LDH activity and ROS content increased, mitochondrial membrane potential decreased compared with the normal control group (P <0.01); 10-7 ~ 10-5mol.L After pretreatment with -1DL, cell survival rate increased, LDH and ROS decreased, mitochondrial membrane potential rose, and in a certain range in a dose-dependent manner. CONCLUSION: DL can protect H2O2-induced oxidative damage in PC12 cells. Its mechanism may be related to the reduction of ROS production and the stabilization of mitochondrial membrane potential.