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Published on: June 30, 2023
[Effect of sodium azide on mitochondrial membrane potential in SH-SY5Y human neuroblastoma cells]
1Department of Pharmacology, Xuan-Wu Hospital, Capital University of Medical Sciences, Beijing Key Laboratory for Brain Aging, Beijing 100053, China. lanizhg@hotmail.com
Objective:
To study the role of mitochondrial deficiency in the pathogenesis of neurodegenerative disease by investigating the energy metabolism in a sodium azide inhibited cytochrome-c oxidase SH-SY5Y Cell model.
Methods:
Human neuroblastoma SH-SY5Y Cells were exposed to sodium azide, then mitochondrial complex IV activity was assayed by microassay method; cell viability was measured by Thiazolyl blue(MTT) method; mitochondrial membrane potential (MMP) was detected by confocal microscopy and flow cytometry.
Results:
Cultured SH-SY5Y cells were exposed to 16-64 mmol/L sodium azide for 1 hour, the mitochondrial complex IV activity decreased dose-dependently. MTT absorbance decreased does- and time-dependently in cultured nerve cells treated by 16-128 mmol/L sodium azide for 1-8 hours. After the treatment of 16 mmol/L sodium azide for 1 hour, both the fluorescence intensity of MMP and normal cell events reduced. Decrease of MMP was significant especially in cell processes.
Conclusion:
Sodium azide induced the impairment of mitochondrial energy synthesis in the cultured nerve cells which is an important cause in cell death.
