西青果多酚对甲基苯丙胺诱导PC12细胞损伤的保护作用及机制

目的:研究西青果多酚对甲基苯丙胺(Methamphetamine,METH)诱导大鼠肾上腺嗜铬细胞瘤(PC12)细胞损伤的保护作用及机制。方法:实验分为对照组、模型组(3 mmol/L METH)和不同浓度西青果多酚组(25、50、100、200 μg/mL西青果多酚+3 mmol/L METH),给药处理24 h后检测细胞存活率、细胞凋亡、细胞DNA损伤、超氧化物歧化酶(Superoxide dismutase,SOD)和谷胱甘肽过氧化物酶(Glutathione peroxidase,GSH-Px)活力以及活性氧(Reactive oxygen species,ROS)和丙二醛(Malondialdehyde,MDA)含量等。结果:与对照组相比,3 mmol/L METH能极显著降低PC12细胞存活率(P<0.01),显著降低SOD和GSH-Px活力(P<0.05),显著增加胞内MDA含量(P<0.05),极显著增加细胞凋亡率、ROS含量和DNA损伤(P<0.01);与模型组相比,50~200 μg/mL西青果多酚能极显著抑制METH诱导的PC12细胞存活率和SOD活力的降低(P<0.01),显著抑制GSH-Px活力下降(P<0.05),极显著抑制METH导致的细胞凋亡、DNA损伤、胞内MDA和ROS含量增加(P<0.01)。结论:西青果多酚对METH诱导的PC12细胞损伤具有明显的保护作用,其作用机制可能与西青果多酚抑制METH诱导的氧化应激,缓解DNA损伤相关。

Protective Effect and Mechanism of Terminalia chebula Polyphenol Extract on Methamphetamine-induced Injury in PC12 Cells

The objective of this work was to study the protective effect and mechanism of Terminalia chebula polyphenol extract(TCPE)on methamphetamine(METH)-induced cell injury in rat pheochromocytoma(PC12)cells. Methods:PC12 cells were divided into control group,model group(3 mmol/L METH)and TCPE-treated groups(25,50,100,200 μg/mL TCPE+3 mmol/L METH). After treatment,the following parameters were measured to detect cell responses which were cell viability,apoptosis,DNA damage,SOD and GSH-Px activities,MDA and ROS contents. Results:Compared with the control group,3 mmol/L METH significantly reduced the survival rate of PC12 cells(P<0.01),SOD and GSH-PX activity(P<0.05),significantly increased MDA content(P<0.05),apoptosis rate,ROS content and DNA damage(P<0.01). Compared with the model group,50~200 μg/mL of TCPE could significantly inhibit the decrease of survival rate and SOD activity of PC12 cells induced by METH(P<0.01),the decrease of GSH-PX activity(P<0.05),and the increase of apoptosis,DNA damage,intracellular MDA and ROS content induced by METH(P<0.01).Conclusion:TCPE has a significant protective effect on METH-induced PC12 cell injury,and its mechanism may be related to its inhibition of METH-induced oxidative stress and DNA damage.