Objective:Mitochondrial dysfunction is evident in the early stage of Alzheimer's disease(AD).Therefore development of drugs that protect mitochondrial function is a promising strategy for AD.The present work was t...Objective:Mitochondrial dysfunction is evident in the early stage of Alzheimer's disease(AD).Therefore development of drugs that protect mitochondrial function is a promising strategy for AD.The present work was to investigate the effects of 2,3,5,4'-Tetrahydroxystilbene-2-O-β-d-glucosides(TSG) on a mitochondrial dysfunction cell model induced by sodium azide and elucidate the underlying mechanisms.Methods:Mitochondrial membrane potential(MMP) was detected by a fluorescence method.Cellular adenosine triphosphate(ATP) level was measured using a firefly luciferase-based kit.Reactive oxygen species(ROS) was detected using dichlorofluorescin diacetate(DCFH-DA).The expression levels of Bcl-2 and Bax were measured by Western blotting assay.Flow cytometry was utilized to measure apoptosis.Results:Pretreatment of TSG(25-200 μmol/L) for 24 h significantly elevated MMP and ATP content,reduced ROS level and Bax/Bcl-2 ratio,and inhibited apoptosis in SH-SY5 Y cells exposed to sodium azide.Conclusion:These results suggest that TSG protects SH-SY5 Y cells against sodium azide-induced mitochondrial dysfunction and apoptosis.These findings are helpful to understand the protective effect of TSG on mitochondria,which are involved in the early stage of AD.展开更多
基金supported by the National Natural Science Foundation of China (Nos.81273498, 81341087)National Science and Technology Major Project of China (No.2015ZX09101-016)。
文摘Objective:Mitochondrial dysfunction is evident in the early stage of Alzheimer's disease(AD).Therefore development of drugs that protect mitochondrial function is a promising strategy for AD.The present work was to investigate the effects of 2,3,5,4'-Tetrahydroxystilbene-2-O-β-d-glucosides(TSG) on a mitochondrial dysfunction cell model induced by sodium azide and elucidate the underlying mechanisms.Methods:Mitochondrial membrane potential(MMP) was detected by a fluorescence method.Cellular adenosine triphosphate(ATP) level was measured using a firefly luciferase-based kit.Reactive oxygen species(ROS) was detected using dichlorofluorescin diacetate(DCFH-DA).The expression levels of Bcl-2 and Bax were measured by Western blotting assay.Flow cytometry was utilized to measure apoptosis.Results:Pretreatment of TSG(25-200 μmol/L) for 24 h significantly elevated MMP and ATP content,reduced ROS level and Bax/Bcl-2 ratio,and inhibited apoptosis in SH-SY5 Y cells exposed to sodium azide.Conclusion:These results suggest that TSG protects SH-SY5 Y cells against sodium azide-induced mitochondrial dysfunction and apoptosis.These findings are helpful to understand the protective effect of TSG on mitochondria,which are involved in the early stage of AD.
