Abstract
Stroke is a leading cause of mortality worldwide, as well as a source of long-term disabilities and huge socioeconomic costs. This study investigates the effects of resveratrol, an antioxidant supplement, on blood pressure, weight status, glucose, and lipid profile in patients who had a stroke in the last 12 months. Two hundred and twenty-eight patients were divided into three groups: group I received only allopathic treatment (control group), while groups II and III received allopathic treatment with a daily supplementation of oral resveratrol (100 and 200 mg, resp.) for 12 months. In all groups, the changes of the studied parameters were monitored at 6 and 12 months from the initial evaluation. In groups II and III, resveratrol induced significant changes (p < 0.05) in the blood pressure, body mass index, as well as all parameters of the lipid profile, and glucose (in nondiabetic patients), compared to the control group. The supplementation of the allopathic treatment with resveratrol had a beneficial effect on all monitored parameters, which serve as major risk factors for stroke.
Highlights
Neurodegenerative, circulatory, and cardiovascular diseases and cancers are considered as direct consequence of the complex of phenomena, named “oxidative stress” [1,2,3]
A recent study has revealed that about 90% of strokes can be attributed to the presence of 10 risk factors, including high blood pressure (BP), dyslipidemias, consumption of toxic substances, obesity, daily stress, sedentariness, and diabetes mellitus [5]
We show that long-term resveratrol supplementation in patients poststroke had a beneficial effect on these parameters that serve as major risk factors for stroke
Summary
Neurodegenerative, circulatory, and cardiovascular diseases and cancers are considered as direct consequence of the complex of phenomena, named “oxidative stress” [1,2,3]. There are cumulative evidences suggesting that ROS can damage the cellular components [8], enhance the production of inflammatory mediators which in turn can lead to additional oxidative stress [9,10,11,12], and are involved in all the pathophysiological stages of neuronal death [13]. Mitochondria (the main ROS-generating cellular components) suffer dysfunction, which causes an increase in oxidative stress. Increased production of ROS through mitochondria plays a role in the pathogenesis of stroke through direct damage to biomolecules resulting in necrosis, necroptosis and apoptosis, damaged endothelium-dependent vasodilator mechanisms, induction of mitochondrial permeability of transition, and interrupted excitation-contraction coupling [14]
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