Pratensein

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.

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.

Chem Biol Interact. 2016 Nov 25;259(Pt B):295-300.

Flavonoids induce the expression of acetylcholinesterase in cultured osteoblasts.[Pubmed: 27019979]

Flavonoids, a group of natural compounds mainly derived from plants, are known to possess osteogenic effects in bone cells.
METHODS AND RESULTS:
Here, we aimed to test if flavonoid could induce a cholinergic enzyme, acetylcholinesterase (AChE), as well as bone differentiation. In cultured rat osteoblasts, twenty flavonoids, deriving from Chinese herbs and having known induction of alkaline phosphatase (ALP1) expression, were tested for its induction activity on AChE expression. Eleven flavonoids showed the induction, and five of them had robust activation of AChE expression, including baicalin, calycosin, genistin, hyperin and Pratensein: the induction of AChE included the levels of mRNA, protein and enzymatic activity. Moreover, the flavonoid-induced AChE expression in cultured osteoblast was in proline-rich membrane anchor (PRiMA)-linked tetrameric globular form (G4) only. In parallel, the expression of PRiMA was also induced by the application of flavonoids. The flavonoid-induced AChE in the cultures was not affected by estrogen receptor blocker, ICI 182,780.
CONCLUSIONS:
Taken together, the induction of PRiMA-linked AChE in osteoblast should be independent to classical estrogen signaling pathway.

Biol Pharm Bull. 2009 Jul;32(7):1289-94.

Characterization of the isoflavone pratensein as a novel transcriptional up-regulator of scavenger receptor class B type I in HepG2 cells.[Pubmed: 19571401]

Scavenger receptor class B type I (SR-BI), as well as its human homologue CLA-1, plays an important role in reverse cholesterol transport (RCT) as high density lipoprotein (HDL) receptor.
METHODS AND RESULTS:
Using a previously developed cell-based screening model for CLA-1 up-regulators, Pratensein, was shown to present activity in elevating CLA-1 transcriptional level. In this study, three other isoflavones including formononetin, genistein and daidzein were also shown to up-regulate CLA-1 transcriptional activity in the cell-based reporter assay. The effects of Pratensein on up-regulating CLA-1 expression were demonstrated at both mRNA and protein levels, and validated by its increasing of 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate-labeled (DiI)-HDL uptake in HepG2 cells. Furthermore, the cis-elements responsible for the Pratensein up-regulatory effects were mapped to the -1055/-182 bp fragment of CLA-1 promoter in HepG2 cells.
CONCLUSIONS:
These findings might provide a new molecular mechanism by which isoflavones potentially prevent atherosclerosis.