| Description: |
Pratensein as a novel transcriptional up-regulator of scavenger receptor class B type I in HepG2 cells. Pratensein has anti-inflammatory activity, it has robust activation of acetylcholinesterase expression, the induction of acetylcholinesterase included the levels of mRNA, protein and enzymatic activity; it can significantly ameliorate Aβ1-42-induced spatial learning and memory impairment through reducing neuroinflammation via inhibition of glial activation and NF-κB activation, and restoring synapse and BDNF levels. |
| Targets: |
AChR | NF-kB | Beta Amyloid | TNF-α | BDNF |
| In vitro: |
| Neurosci Res. 2008 Oct;62(2):123-30. | | Protective effect of isoflavones from Trifolium pratense on dopaminergic neurons.[Pubmed: 18675857 ] |
METHODS AND RESULTS:
In the present study, protective effect of five isoflavones (formononetin, daidzein, pratensein, calycosin and irilone) from Trifolium pratense on lipopolysaccharide-induced dopaminergic neurodegeneration was studied for the first time. The results showed that all five isoflavones attenuated LPS-induced decrease in dopamine uptake and the number of dopaminergic neurons in a dose-dependent manner in rat mesencephalic neuron-glia cultures. Moreover, they also significantly inhibited LPS-induced activation of microglia and production of tumor necrosis factor-alpha, nitric oxide and superoxide in mesencephalic neuron-glia cultures and microglia-enriched cultures. In addition, the rank order of protective potency of five isoflavones was: pratensein>daidzein>calycosin>formononetin>irilone.
CONCLUSIONS:
This study suggested that all five isoflavones protected dopaminergic neurons against LPS-induced injury through inhibition of microglia activation and proinflammatory factors generation. |
|
| In vivo: |
| Neurosci Lett. 2015 Apr 10;592:48-53. | | Pratensein ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels.[Pubmed: 25748315 ] | This study was designed to investigate the protective effect of pratensein against cognitive impairment induced by amyloid beta (1-42) (Aβ1-42) in rats.
METHODS AND RESULTS:
Aβ1-42 peptide was injected bilaterally in the hippocampus of rat. Next, pratensein was administered orally for 3 weeks. Our findings demonstrated that treatment with pratensein ameliorated learning and memory deficits in Aβ1-42 rat model of AD. Pratensein treatment significantly attenuated neuronal degeneration and apoptosis in hippocampus. Moreover, the over-expression in IL-1β and TNF-α as well as the extensive astrogliosis and microgliosis in hippocampus induced by Aβ1-42 were significantly reduced following administration of pratensein. Concomitantly, pratensein treatment significantly suppressed the activation of NF-κB in hippocampus. In addition, pratensein was able to increase the levels of synaptophysin and brain-derived neurotrophic factor (BDNF).
CONCLUSIONS:
These results indicate that pratensein could significantly ameliorate Aβ1-42-induced spatial learning and memory impairment through reducing neuroinflammation via inhibition of glial activation and NF-κB activation, and restoring synapse and BDNF levels, suggesting that administration of pratensein could likely provide a therapeutic approach for AD. |
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