Abstract
Polyphenols are an important family of molecules of vegetal origin present in many medicinal and edible plants, which represent important alimentary sources in the human diet. Polyphenols are known for their beneficial health effects and have been investigated for their potential protective role against various pathologies, including cancer, brain dysfunctions, cardiovascular diseases and stroke. The prevention of stroke promoted by polyphenols relies mainly on their effect on cardio- and cerebrovascular systems. However, a growing body of evidence from preclinical models of stroke points out a neuroprotective role of these molecules. Notably, in many preclinical studies, the polyphenolic compounds were effective also when administered after the stroke onset, suggesting their possible use in promoting recovery of patients suffering from stroke. Here, we review the effects of the major polyphenols in cellular and in vivo models of both ischemic and hemorrhagic stroke in immature and adult brains. The results from human studies are also reported.
Highlights
The Burden of StrokeStroke is a cerebrovascular disease caused by the interruption of blood flow to the brain due to the blockage or rupture of a vessel and can affect both immature and mature brains.Perinatal stroke occurs between the 20th week of gestation and the 28th day after birth with an incidence between 1/2300 and 1/5000 live births [1,2]
The major part of polyphenols exists in plants as glycosides, where different sugars are bonded to the polyphenolic structure in different positions
The incomplete list of polyphenols active in cellular and animal models presented here strongly supports the potential role of many classes of polyphenols against different types of stroke
Summary
Stroke is a cerebrovascular disease caused by the interruption of blood flow to the brain due to the blockage or rupture of a vessel and can affect both immature and mature brains. In the major part of cases, SAH is caused by the rupture of an intracranial aneurysm [17] Stroke in both immature and mature brains is a complex phenomenon that includes a series of pathological processes such as excitotoxicity, oxidative damage, apoptosis and inflammation, which eventually leads to cell death [18,19,20]. One of the main pathophysiological features of ischemic stroke is the brain–blood barrier (BBB) disruption, an event that occurs in almost two-thirds of patients in the first hours from the ischemia onset and causes vasogenic edema, hemorrhagic transformation and increased mortality [21,22]. In light of the above considerations, there is an urgent need for the development of new therapies able to prevent or reduce stroke neuronal injury
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