Neuroprotection by the soy isoflavone, genistein, via inhibition of mitochondria-dependent apoptosis pathways and reactive oxygen induced-NF-κB activation in a cerebral ischemia mouse model

Only three years old and I bet your doctor and hospital have not done one fucking thing to help your recovery based upon this research. What is the downside even though this is only in mice? Are your doctors waiting for clinical human studies before they do anything? Stroke survivors will never get better if we don't have any doctors willing to show some initiative and try new stuff based upon research. They can have you sign a waiver stating you won't sue them for feeding you soybeans. So much that can be done for survivors and no one even trying to help them. And you wonder why I'm angry all the time. I fucking hate stupid people. Lazy people even more.
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.

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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.