Effect of edaravone on mitochondrial function during ketamine-induced apoptosis in PC12 cells / 中华麻醉学杂志
Chinese Journal of Anesthesiology
; (12): 1101-1104, 2021.
Article
em Zh
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| ID: wpr-911325
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WPRO
ABSTRACT
Objective:To evaluate the effect of edaravone on mitochondrial function during ketamine-induced apoptosis in PC12 cells.Methods:Nerve growth factor (NGF)-induced differentiating PC-12 cells were divided into 3 groups ( n=30 each) using a random number table method: control group (group C), ketamine group (group K) and edaravone plus ketamine group (group EK). Cells in group C were commonly cultured.In group K, PC12 cells were incubated with PBS and 100 μmol/L ketamine at 7 days after differentiation.In group EK, cells were incubated with 10 μmol/L edaravone and 100 μmol/L ketamine.The cell viability, caspase-3/7 activity, reactive oxygen species (ROS) activity, adenosine triphosphate (ATP) content and NADH/NAD + ratio were determined using analysis kits at 24 h of incubation.The cell apoptosis was observed by TUNEL assay and apoptosis rate was calculated. Results:Compared with group C, the cell viability, caspase-3/7 activity, NADH/NAD + ratio and apoptosis rate were significantly increased, and ROS activity and ATP content were decreased in group K ( P<0.05). Compared with group K, the cell viability, caspase-3/7 activity, NADH/NAD + ratio and apoptosis rate were significantly decreased, and ROS activity and ATP content were increased in group EK ( P<0.05). Conclusion:The mechanism by which edaravone inhibits ketamine-induced apoptosis in PC12 cells is related to improving mitochondrial function.
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WPRIM
Idioma:
Zh
Revista:
Chinese Journal of Anesthesiology
Ano de publicação:
2021
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Article