Pratensein, a flavonoid, ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels^[1].

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].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

300.26

C₁₆H₁₂O₆

2284-31-3

Room temperature in continental US; may vary elsewhere.

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• [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.