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目的探讨樟芝酵素对苯丙胺致PC12细胞损伤的保护作用及其机理。方法利用PC12细胞模型,设置对照组,3.5 mmol/L苯丙胺组和3.5 mmol/L苯丙胺+樟芝酵素组。(1)通过显微镜观察细胞形态的变化;(2)通过MTT法检测细胞存活率;(3)通过Western blot分析Caspase-3的变化;(4)通过流式细胞仪检测细胞凋亡和细胞内活性氧的变化。结果 (1)苯丙胺损伤了PC12细胞的结构,导致细胞凋亡增加,樟芝酵素能够减少细胞的凋亡,提高细胞的存活率;(2)樟芝酵素减少了细胞内ROS的生成;(3)樟芝酵素组procaspase-3(35 kd)蛋白含量比苯丙胺组增多,激活分子caspase-3(17 kd)含量较苯丙胺组减少。结论樟芝酵素对苯丙胺致PC12细胞毒性损伤具有保护作用,其机理与抑制细胞线粒体凋亡信号通路以及减少细胞内氧自由基的产生密切相关。
Objective To investigate the protective effect and mechanism of Campylobacter on amphetamine-induced PC12 cell injury. Methods The PC12 cell model was used to establish the control group, 3.5 mmol / L amphetamine group and 3.5 mmol / L amphetamine + campylobacter enzyme group. (1) The morphological changes of the cells were observed with a microscope; (2) Cell viability was detected by MTT assay; (3) Caspase-3 changes were analyzed by Western blot; (4) Flow cytometry was used to detect apoptosis and intracellular Changes in reactive oxygen species. Results (1) Amphetamine damage the structure of PC12 cells, leading to increased apoptosis, Campylobacter enzyme can reduce cell apoptosis and improve cell survival rate; (2) Campylobacter enzyme reduces intracellular ROS generation; (3) ) The content of procaspase-3 (35 kd) in camphor enzyme group was higher than that in amphetamine group, and the content of active protein caspase-3 (17 kd) was lower than that in amphetamine group. CONCLUSION: Campylobacter zymosan could protect PC12 cells against toxicity caused by amphetamine and its mechanism is closely related to the inhibition of mitochondrial apoptosis signaling pathway and the reduction of intracellular oxygen free radicals.