But this might be difficult because you have to know 14 days before your stroke so you can start pretreatment. This would then require research showing if this is helpful treating poststroke. So much research to do and no one to do it.
http://www.ncbi.nlm.nih.gov/m/pubmed/22490611/?i=6&from=soy%20stroke
Qian Y, et al. Neurochem Int. 2012.
Abstract
Recently,
the treatment of stroke has focused on antioxidant therapies, where
oxidative stress is implicated. The preventive and therapeutic potential
of plant compounds on ischemic stroke has been intensively studied
because many of them contain antioxidant properties. Genistein, one of
the active ingredients in soybean, possesses many bioactivities. In this
study, we investigated the potential neuroprotective effects of
genistein and its possible mechanism of action in a cerebral ischemia
mouse model. Mice were pretreated with genistein (2.5, 5, and 10mg/kg)
or vehicle orally once daily for 14 consecutive days before transient
middle cerebral artery occlusion was performed. Genistein at doses of
2.5-10mg/kg significantly reduced the infarct volume, improved the
neurological deficit and prevented cell apoptosis after ischemia. In
addition, genistein pretreatment was shown to inhibit the
ischemia-induced reactive oxygen species (ROS) production, enhance the
activities of antioxidant enzymes superoxide dismutase (SOD) and
glutathione peroxidase (GPx), and decrease levels of malondialdehyde
(MDA) in stroke mice. Moreover, genistein reversed the mitochondria
dysfunction after ischemia, as evidenced by decreasing mitochondria ROS
levels, preventing cytochrome C release to the cytoplasm and inhibiting
caspase-3 activation. Western blotting showed ischemia activated the
ROS-dependent nuclear factor-κB (NF-κB) signaling pathway, and genistein
suppressed phosphorylation and activation of the NF-κB p65 subunit, as
well as the phosphorylation and degradation of the inhibitor protein of
κBα (IκBα). Our findings suggested that genistein has a neuroprotective
effect in transient focal ischemia, which may involve regulation of
mitochondria-dependent apoptosis pathways and suppression of ROS-induced
NF-κB activation.
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