Effects of tetrahydroxystilbene glucoside in Parkinson′s disease mice model induced by MPTP

OBJECTIVE To observe effects of tetrahydroxystilbene glucoside(TSG)on behavior,content of dopamine and its metabolites in striatum of Parkinson′s disease(PD)model mice induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)injection.METHODS Mice were randomly divided into control group,model group,TSG low dose(60mg·kg-1)and high dose(120mg·kg-1)groups.The behavior changes of mice were observed by pole test,rotarod test and spontaneous movement test.The tyrosine hydroxylase(TH)positive cells were detected by immunohistochemical method.The content of dopamine(DA)and its metabolites in striatum were determined by HPLC-ECD.RESULTS MPTP model mice showed behavior deficit.The number of TH positive neurons in substantia nigra,the content of dopamine and its metabolites in striatum in model mice decreased significantly compared with control group.TSG ameliorated mice behavior,increased the number of TH positive neurons in the substantia nigra about 18.8%,and elevated the content of dopamine in striatum about 34.5% compared with model mice.CONCLUSION TSG protected dopaminergic neurons against MPTP-induced damage,and may become a candidate drug for prevention and treatment of Parkinson′s disease.

Tetrahydroxystilbene glucoside protects against sodium azide-induced mitochondrial dysfunction in human neuroblastoma cells

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.