White crystalline powder
3-O-[(2E)-3-(4-Hydroxy-3,5-dimethoxyphenyl)-2-propenoyl]-β-D-fructofuranosyl 6-O-[(2E)-3-(4-hydroxy-3,5-dimethoxyphenyl)-2-propenoyl]-α-D-glucopyranoside/(3-Sinapoyl)fructofuranosyl-(6-sinapoyl)glucopyranoside/3',6-Disinapoylsucrose/3,6'-di-O-sinapoylsucrose/3-SF-6-Sglu/α-D-Glucopyranoside, 3-O-[(2E)-3-(4-hydroxy-3,5-dimethoxyphenyl)-1-oxo-2-propen-1-yl]-β-D-fructofuranosyl 6-O-[(2E)-3-(4-hydroxy-3,5-dimethoxyphenyl)-1-oxo-2-propen-1-yl]-/Disinapoyl Sucrose, 3,6'-
988.0±65.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:139891-98-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
3,6′-Disinapoyl sucrose (DISS) is an oligosaccharide ester natural product originating from the root of wild Polygala tenuifolia. Our previous reports suggested that DISS can have neuroprotective effects and antidepressive activity in rats, at least in part, by increased expression of cyclic AMP response element (CRE)-binding protein (CREB) and its downstream target protein, brain-derived neurotrophic factor (BDNF). The aim of the present study was to explore the mechanism of DISS-modulated BDNF and CREB expression. In this study, we confirmed its neuroprotective effect by showing that DISS, at concentrations above 30 μM, could promote the neuron cell viability and protected the glutamate and H2O2-induced toxicity in the human neuroblastoma (SH-SY5Y) cell line. DISS treatment also increased acute (from 15 to 30 min) BDNF expression and CREB phosphorylation in a dose-dependent manner. Pharmacological inhibition of mitogen-activated protein kinase 1 (ERK1/2), CaMKII, and Trk (with U0126, KN93, or K252a, respectively) partially attenuated the stimulatory effect of DISS on phospho-CREB and BDNF expression; however, it was not inhibited by pharmacological inhibition of PKA or PI3K (with H89 and LY294002, respectively). The results are consistent with the effects of DISS on CRE-directed gene transcription, as U0126 and KN-93 treatment also blocked the DISS-induced expression of the CRE-luciferase reporter gene. The results from the present study suggest that DISS-mediated regulation of BDNF gene expression is associated with CREB-mediated transcription of BDNF and upstream activation of ERK1/2 and CaMKII. Finally, DISS may exert neuroprotective and antidepressant effects through these signaling pathways in neuronal cells.
Neuroprotective Effects of 3,6'-disinapoyl Sucrose Through Increased BDNF Levels and CREB Phosphorylation via the CaMKII and ERK1/2 Pathway
Yuan Hu 1 , Ming-Yue Liu, Ping Liu, XianZhe Dong, Aislyn D W Boran
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.
Protection of SH-SY5Y Neuronal Cells From Glutamate-Induced Apoptosis by 3,6'-disinapoyl Sucrose, a Bioactive Compound Isolated From Radix Polygala
Yuan Hu 1 , Jie Li, Ping Liu, Xu Chen, Dai-Hong Guo, Qing-Shan Li, Khalid Rahman
Recent studies suggest that the behavioral effects of chronic antidepressant treatment are mediated by stimulation of hippocampal neuronal plasticity and neurogenesis. The present study was designed to examine the effects of 3,6′-disinapoyl sucrose (DISS), a bioactive component of Polygala tenuifolia Willd, on the expressions of four plasticity-associated genes: cell adhesion molecule L1 (CAM-L1), laminin, cAMP response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in hippocampus, all of which are involved in neuronal plasticity and neurite outgrowth. We confirmed that chronic stress in rats caused a reduction in sensitivity to reward (sucrose consumption) and a decrease in mRNA levels of CAM-L1, laminin, and BDNF, together with a decrease in protein levels of phosphorylated CREB and BDNF. Repeated administration of DISS for 21 days at doses of 5, 10 and 20mg/kg reversed stress-induced alterations in sucrose consumption and these target mRNA and protein levels. In conclusion, increased expressions in the hippocampus of three noradrenergic-regulated plasticity genes and one neurotrophic factor may be one of the molecular and cellular mechanisms underlying the antidepressant action of DISS in chronic mild stress (CMS) rats.
Antidepressant-like Effects of 3,6'-disinapoyl Sucrose on Hippocampal Neuronal Plasticity and Neurotrophic Signal Pathway in Chronically Mild Stressed Rats
Yuan Hu 1 , Hong-Bo Liao, Guo Dai-Hong, Ping Liu, Yu-Yu Wang, Khalid Rahman
3',6-Disinapoylsucrose, the index component of Yuanzhi (Polygala tenuifolia Willd), possesses potent antioxidant activity and antidepressant effect.