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Pueraria Mirifica initiative promotes the cellular mechanism of neuronal survival in neuron human neuroblastoma cells.Authors: Sayan Sawatsri*1, Wanphen Yamkunthong1, Neil Sidell2.
1. Phramongkutklao Hospital and College of Medicine, Bangkok, Thailand;
2. Emory University School of Medicine, GYN-OB Dept., Research Div., Atlanta, GA, USA.
Pueraria Mirifica (PM) or White Kwao Krue (Thai Herb) has been used as a rejuvenator for long time in aging. It contains a variety of phytoestrogens that possess the highest estrogenic activity. In molecular research and epidemiological data show that estrogen replacement therapy (ERT) can decrease the risk of developing Alzheimer's disease. Interestingly, whether the estrogenic effect of PM can prevent neurotrophic from neurotoxic agents e.g. glutamate, H2O2, and beta-amyloid 25-35 in AD model. What a mechanism of PM that prevents neuronal cell death is.
Objectives: The current study investigated the neurotrophic and neuroprotective action of the complex formulation of phytoestrogen from a standardized PM extract compare with 17b-estradiol in AD model in vitro.
Methods: Crude PM was extracted by ethanol and standardized by HPLC. Action of standarize PM was pretreated in human neuroblastoma cell line (LA-N5) in complete media of estrogen deprivation condition with neurotoxic agents; 0.2mM glutamate, 20µM H2O2, and 8 µg/ml beta-amyloid 25-35 by inhibit cell death. By using inverted microscope, morphologic and biochemical analysis were conducted in neuroblastoma cultures to determine the neurotrophic and neuroprotective properties of standardize PM and 17b-estradiol. Using ICI anti-estrogenic activity and estrogen dependent breast cancer cell for demonstrate the inhibition of PM in estrogen receptor pathway in AD model.
Results: the results demonstrated that PM significantly decreased neuronal cell death in a time and dose dependent fashion. Results of neuroprotection studies demonstrated that PM and 10-8 M 17b-estradiol induced highly significant neuroprotection against beta-amyloid, hydrogen peroxide, glutamate-induced toxicity. Inhibi action of PM and 17b-estradiol by estrogen antagonist (ICI164,384) after induce with neurotoxic agents that show significantly increase cell death.
Conclusions: PM shows estrogenic activity similar 17b-estradiol and prevents neurotoxic agents for neuronal dead significantly by may pass estrogen pathway. For clinical application of PM possible to use for intervention in Alzheimer's disease and other neurodegenerative disease in aging in the near future.
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