| Identification | Back Directory | [Name]
PRATENSEIN | [CAS]
2284-31-3 | [Synonyms]
PRATENSEIN
PRALENREIN
OROBOL 4'-METHYL ETHER
PATCHOULI ALCOHOL (RG)
4'-METHOXY-3',5,7-TRIHYDROXYISOFLAVONE
5,7,3'-Trihydroxy-4'-methoxyisoflavone
5,7-Dihydroxy-3-(3-hydroxy-4-methoxyphenyl)-4H-1-benzopyran-4-one | [Molecular Formula]
C16H12O6 | [MDL Number]
MFCD00210594 | [MOL File]
2284-31-3.mol | [Molecular Weight]
300.26 |
| Chemical Properties | Back Directory | [Melting point ]
272-273° | [Boiling point ]
576.7±50.0 °C(Predicted) | [density ]
1.512±0.06 g/cm3(Predicted) | [form ]
Solid | [pka]
6.45±0.20(Predicted) | [color ]
White to off-white | [InChI]
InChI=1S/C16H12O6/c1-21-13-3-2-8(4-11(13)18)10-7-22-14-6-9(17)5-12(19)15(14)16(10)20/h2-7,17-19H,1H3 | [InChIKey]
FPIOBTBNRZPWJW-UHFFFAOYSA-N | [SMILES]
C1OC2=CC(O)=CC(O)=C2C(=O)C=1C1=CC=C(OC)C(O)=C1 |
| Hazard Information | Back Directory | [Uses]
Pratensein, a flavonoid, ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels[1]. | [Definition]
ChEBI: A member of the class of 7-hydroxyisoflavones in which isoflavone is substituted by hydroxy groups at the 5, 7, and 3' positions, and by a methoxy group at the 4' position. | [in vivo]
Pratensein significantly attenuates neuronal degeneration and apoptosis in hippocampus. The over-expression in IL-1β and TNF-α as well as the extensive astrogliosis and microgliosis in hippocampus induced by Aβ1-42 are significantly reduced following administration of Pratensein. Pratensein treatment significantly suppresses the activation of NF-κB in hippocampus. Pratensein is able to increase the levels of synaptophysin and brain-derived neurotrophic factor (BDNF)[1].
Pratensein (20 mg/kg; p.o.; once daily for 3 weeks) ameliorates learning and memory deficits in Aβ1-42 rat model of Alzheimer’s disease[1]. | Animal Model: | Male 10-week old Wistar rats[1] | | Dosage: | 20 mg/kg | | Administration: | P.o.; once daily for 3 weeks | | Result: | The spatial learning and memory ability of rats was improved.
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| [References]
[1] Liang C, et al. Pratensein ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels. Neurosci Lett. 2015;592:48-53. DOI:10.1016/j.neulet.2015.03.003 |
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