Wednesday, January 25, 2012

Angiogenesis at short and longer intervals post ischemia: Relationship to neuroprotective actions of resveratrol

So does this mean wine would be good for you to protect against the cascade of death?
Ask your doctor. I can just see the ER nurses feeding you wine while still in the ICU.
Ok, not viable, in the order of one milligram per glass. From the 2011 Canadian Stroke Congress.
page 127 here:
http://www.strokecongress.org/2011/wp-content/uploads/2011/12/CSC_Abstracts.pdf
Background: Angiogenesis, or the formation of new blood vessels, is an essential element of brain developmentand health. Resveratrol (RSV) is a naturally occurring polyphenol phytoalexin that has an array of beneficial health effects and that has been shown to protect the brain against ischemic injury. However, whether
protection at the neuronal level is associated with plastic changes in brain organization post stroke or with recovery from cognitive impairments remains unknown. The present study examined the effects of 21-day RSV pre-treatment (1 or 10 mg/kg dose; i.p.) on ischemia-induced CA1 neuronal cell loss, angiogenesis levels in the hippocampus and behavioural impairment following 10 min global ischemia at 7 and 85 days post ischemia.
Methods: Male Wistar rats were divided into five groups, namely, sham + saline, ischemia + saline, ischemia + 1 mg/kg RSV, ischemia + 10 mg/kg RSVand sham + 10 mg/kg RSV. 7 or 85 days post surgery, brains were perfused and histopathological damage in the hippocampus determined. Immunohistochemical assessment of angiogenesiswas performed using Endothelial cell adhesion molecule-1 (CD-31)-labelling of blood vessels. Spatial working and reference memory were assessed using delayed non-matching or matching radial arm maze tasks.
Results: Our findings indicated significant neuroprotection by RSV at both time points investigated. Behaviorally, administration of 10 mg/kg RSV failed to improve ischemia-induced spatial memory deficits on either of the maze tasks, suggesting dose-dependent effect of RSV. We also show an increase in CD-31 expression in RSVtreated compared to saline-treated ischemic rats 7 and 85 days post injury. Noteworthy, angiogenesis was not restricted to areas most affected by ischemic injury (i.e., CA1 layer), suggesting complex relationships between angiogenesis and stroke recovery. Conclusion: This study demonstrates that RSV has the ability to protect CA1
neurons against ischemic injury, a phenomenon possibly promoted by increased angiogenesis.

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