| Bioactivity | Pratensein, a flavonoid, ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels[1]. |
| 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: |
| Name | Pratensein |
| CAS | 2284-31-3 |
| Formula | C16H12O6 |
| Molar Mass | 300.26 |
| Appearance | Solid |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | -20°C, sealed storage, away from moisture and light *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light) |
| Reference | [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. |