Publication | Open Access
Protection of SH-SY5Y Neuronal Cells from Glutamate-Induced Apoptosis by 3,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msup><mml:mn mathvariant="bold">6</mml:mn><mml:mo>′</mml:mo></mml:msup></mml:math>-Disinapoyl Sucrose, a Bioactive Compound Isolated from Radix Polygala
311
Citations
12
References
2011
Year
Glutamate ToxicityApoptosisCell DeathSh-sy5y Neuronal CellsCellular PharmacologyPharmacotherapyExperimental PharmacologyMolecular PharmacologyNeurologyRadix PolygalaNeuroimmunologyNeurochemistryGlutamate-induced ApoptosisMolecular NeuroscienceBiochemistryMedicineNeuropharmacologyNeuroprotectionPharmacologyMolecular Neurobiology3,6'-Disinapoyl SucroseDrug Discovery
The neuroprotective effects of 3,6'-disinapoyl sucrose (DISS) from Radix Polygala against glutamate-induced SH-SY5Y neuronal cells injury were evaluated in the present study. SH-SY5Y neuronal cells were pretreated with glutamate (8 mM) for 30 min followed by cotreatment with DISS for 12 h. Cell viability was determined by (3,4,5-dimethylthiazol-2-yl)-2,5-diphenylte-trazolium bromide (MTT) assay, and apoptosis was confirmed by cell morphology and flow cytometry assay, evaluated with propidium iodide dye. Treatment with DISS (0.6, 6, and 60 μmol/L) increased cell viability dose dependently, inhibited LDH release, and attenuated apoptosis. The mechanisms by which DISS protected neuron cells from glutamate-induced excitotoxicity included the downregulation of proapoptotic gene Bax and the upregulation of antiapoptotic gene Bcl-2. The present findings indicated that DISS exerts neuroprotective effects against glutamate toxicity, which might be of importance and contribute to its clinical efficacy for the treatment of neurodegenerative diseases.
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