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Mood disorders occur in 30% of stroke patients, and of these post-stroke depression (PSD) is the most significant. This study aimed to evaluate the antidepressive-like effects and in vivo antioxidant activity of a chemically characterized maqui berry (Aristotelia chilensis (Molina) Stuntz) extract obtained from an optimized extraction method, on a murine PSD model. The extraction process was optimized to maximize anthocyanin content, and the phytochemical profile of the extract was evaluated using a multi-methodological approach including a liquid chromatographic method coupled with mass spectrometry and nuclear magnetic resonance spectroscopy. The antidepressive-like activity was investigated through despair swimming and tail suspension tests. The in vivo antioxidant activity was evaluated in mouse brain tissue by measuring the activity of antioxidant enzymes and lipid peroxidation products. A number of compounds have been first identified in maqui berry here, including malvidin-glucoside, GABA, choline and trigonelline. Moreover, the results showed that the antidepressive-like activity exerted by the extract, which was found to restore normal mouse behavior in both despair swimming and tail suspension tests, could be linked to its antioxidant activity, leading to the conclusion that maqui berries might be useful for supporting pharmacological therapy of PSD by modulating oxidative stress., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Autophagy is an important biological mechanism involved in the regulation of numerous fundamental cellular processes that are mainly associated with cellular growth and differentiation. Autophagic pathways are vital for maintaining cellular homeostasis by enhancing the turnover of nonfunctional proteins and organelles. Neuronal cells, like other eukaryotic cells, are dependent on autophagy for neuroprotection in response to stress, but can also induce cell death in cerebral ischemia. Recent studies have demonstrated that autophagy may induce neuroprotection following acute brain injury, including ischemic stroke. However in some special circumstances, activation of autophagy can induce cell death, playing a deleterious role in the etiology and progression of ischemic stroke. Currently, there are no therapeutic options against stroke that demonstrate efficient neuroprotective abilities. In the present work, we will review the significance of autophagy in the context of ischemic stroke by first outlining its role in ischemic neuronal death. We will also highlight the potential therapeutic applications of pharmacological modulators of autophagy, including some naturally occurring polyphenolic compounds that can target this catabolic process. Our findings provide renewed insight on the mechanism of action of autophagy in stroke together with potential neuroprotective compounds, which may partially exert their function through enhancing mitochondrial function and attenuating damaging autophagic processes.

Hypericum androsaemum L., commonly known as 'tutsan' or 'shrubby St. John's Wort', is a member of the Hypericum genus found growing spontaneously in the Mediterranean area and is cultivated extensively as an ornamental plant due to the showy color variation in its fresh berry-like capsules, which turn from red to shiny black as they ripen. Tutsan has also been used in Portuguese and Spanish folk medicine to treat depression. In this study, we assessed the beneficial role of the water extract of H. androsaemum red berries (WE) in an experimental animal model of post-stroke depression. WE was obtained by decoction of H. androsaemum red berries, and its content of ten bioactive compounds was determined through HPLC-DAD analysis. Behavioral tests were carried out using a mouse model of post stroke depression to examine the antidepressive-like activity of WE at two doses (15 and 30 mg/kg bw). In addition, the in vivo antioxidant activity in the mouse brain was evaluated by measuring CAT, GSH, and SOD activity and TBARS levels. WE contained significant amounts of shikimic acid (110.0 g/kg), chlorogenic acid (56.9 g/kg), catechin (5.8 g/kg) and hyperoside (2.7 g/kg). Overall, the highest dosage of WE was found to significantly reduce the symptoms of depression, restoring normal behaviour and reducing levels of oxidative stress by increasing endogenous antioxidant defenses. The protective effects of WE in post-stroke depression in a mouse model were demonstrated in vivo for the first time, and correlated with the antioxidant capacity of its bioactive constituents., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Gallic acid (3,4,5-trihydroxybenzoic acid, GA) is a plant secondary metabolite, which shows antioxidant activity and is commonly found in many plant-based foods and beverages. Recent evidence suggests that oxidative stress contributes to the development of many human chronic diseases, including cardiovascular and neurodegenerative pathologies, metabolic syndrome, type 2 diabetes and cancer. GA and its derivative, methyl-3-O-methyl gallate (M3OMG), possess physiological and pharmacological activities closely related to their antioxidant properties. This paper describes the antidepressive-like effects of intraperitoneal administration of GA and two synthetic analogues, M3OMG and P3OMG (propyl-3-O-methylgallate), in balb/c mice with post-stroke depression, a secondary form of depression that could be due to oxidative stress occurring during cerebral ischemia and the following reperfusion. Moreover, this study determined the in vivo antioxidant activity of these compounds through the evaluation of superoxide dismutase (SOD) and catalase (Cat) activity, thiobarbituric acid-reactive substances (TBARS) and reduced glutathione (GSH) levels in mouse brain. GA and its synthetic analogues were found to be active (at doses of 25 and 50 mg/kg) in the modulation of depressive symptoms and the reduction of oxidative stress, restoring normal behavior and, at least in part, antioxidant endogenous defenses, with M3OMG being the most active of these compounds. SOD, TBARS, and GSH all showed strong correlation with behavioral parameters, suggesting that oxidative stress is tightly linked to the pathological processes involved in stroke and PSD. As a whole, the obtained results show that the administration of GA, M3OMG and P3OMG induce a reduction in depressive symptoms and oxidative stress.

Scope: Growing evidence suggests that oxidative stress plays a role in the development of chronic diseases such as cardiovascular disease and some psychiatric disorders. Tea consumption exerts beneficial effects against damage induced by cerebral ischemia-reperfusion in ischemic stroke and depressive symptoms in depression. The aim of this study was to evaluate, in vivo, the protective activity of green tea (GT) and GABA green tea (GGT) against post-stroke depression (PSD), a common consequence of stroke., Methods and Results: The antidepressive-like effects of GT and GGT were determined by behavioral tests in a mouse model of post-stroke depression. The antioxidant activity was evaluated by GSH, SOD, and TBARS measurements on mouse brain. The chemical composition of tea extracts was characterized through chromatographic methods. GGT and GT resulted active in the modulation of depressive symptoms and the reduction of oxidative stress, restoring normal behavior, and at least in part, antioxidant endogenous defenses. The higher polyphenol, theanine, glutamine, and caffeine content may justify the higher activity found in GGT., Conclusions: This work represents the first attempt to demonstrate the positive effect of tea, and especially GGT, on post-stroke depression and to correlate this effect with the antioxidant activity and phytochemical composition of tea., (© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Extensive evidences has shown the promising effects of Ginkgo biloba consumption on several diseases such as Alzheimer's and Parkinson's diseases, and ischemic stroke, etc. Several studies also have reported its beneficial role on motor activity and cognitive functions. This species contain a unique class of diterpenes, namely Ginkgolide B, which possess several pharmacological activities such as protective effect against cardiovascular disease; the most important causes of death worldwide. The promising effects of Ginkgolide B on stroke, both ischemic and hemorrhagic, are suggested by an overwhelming body of scientific evidences. Many studies have shown that the increase of sirt1 expression, the suppression of nuclear factor kappa-B (NF-kB, the inhibition of the PI3K/Akt pathway and toll-like receptor 4 (TLR4/NF-kB, the up-regulation of heme oxygenase 1, erythropoietin secretion and anti-apoptotic protein expression, the inhibition of pro-apoptotic proteins expression, and the improvement of endothelial NO synthesis are the main molecular mechanisms involved in the protective effect of Ginkgolide B on ischemic stroke. In this review, all the available data on the chemistry, mechanisms of neuroprotection and clinical impacts of Ginkgolide B are critically discussed.

In last decades, diet and dietary components have been regarded as important strategies to prevent the development or mitigate numerous chronic diseases, including inflammation, cardiovascular pathologies, cancer, etc. One of the most common dietary components of Asian population is soy. A plethora of research shows the promising effect of soy soy-based foodstuffs and genistein, which is one of the predominant isoflavone compounds, in the prevention and mitigation of stroke. Growing evidence shows that genistein, which is a selective estrogen receptor modulator, mitigates ischemic stroke-induced damages through the modification of oxidative stress and molecular pathways. The promising pharmacological role of genistein is attributed to its ability to suppress nuclear factor (NF)-kappa B and Akt signaling pathway, direct antioxidant action, and targeting estrogen and androgen-mediated molecular pathways which help to mitigate stroke damages and prolong cell survival. In this work, we systematically review the current reports on the therapeutic role of genistein against ischemic stroke and its molecular mechanism of actions.

Post-stroke depression is a common neuropsychiatric affective disorder that may develop after a stroke event. In addition to abnormalities in the biogenic amine neurotransmitters and cytokine expression induced by stroke we will focus on the role of oxidative stress and hypothesize that polyphenols may be useful as therapeutics targets for the treatment of post-stroke depression. In this paper, we discuss the hypothesis that increased oxidative stress in cerebral tissues during ischemia is implicated in the pathogenesis of depressive-like symptoms following stroke. There is substantive evidence regarding the role of oxidative stress in the pathogenesis of both stroke and depression, which provides support to this hypothesis. Reactive oxygen species, generated during stroke, cause oxidative stress, lipid peroxidation, protein oxidation, and DNA damage in neural tissues. The resultant pathophysiological processes in the neural tissues could be considered a leading mechanism in the induction of post-stroke depression. Antioxidants including polyphenols therefore, may play an important role in the outcomes of ischemia and stroke, due to their ability to protect neurons against oxidative stress, to mitigate ischemic damage via inhibition of lipid peroxidation and ability to interact with the generation of nitric oxide from the vascular endothelium, and also to decrease inflammation. These data suggest that polyphenols may therefore be a useful new therapeutic target for the treatment of post-stroke depression.

Stroke is one of the most common cardiovascular diseases and is known as a leading cause of death in the world. Despite to its high prevalence, there are limited effective therapeutic strategies for stroke till now. However, oxidative stress plays an important role in the pathogenesis of stroke and therefore, antioxidant therapy could be used as a new therapeutic strategy. Among the antioxidants, some natural compounds are very interesting due to their low adverse effects. Resveratrol (3, 5, 4'-trihydroxystilbene) is a natural polyphenolic antioxidant found in grape skin, grape products, and peanuts as well as in red wine. In recent years, much attention has been paid to resveratrol due to its wide range of antioxidant actions. Resveratrol possesses cardioprotective actions through stimulation of nitric oxide production as well as antioxidative and anti-inflammatory effects. Here we review the available literatures on beneficial role of resveratrol on ischemic stroke. We also provide information about chemistry, sources, bioavailability, as well as clinical impacts of resveratrol.

Post-stroke depression is an important psychological consequence of ischemic stroke, and affects around one third of stroke patients at any time post-stroke. It has a negative impact on patient morbidity and mortality, and as such development of effective post-stroke recognition and treatment strategies are very important. There are several therapeutic strategies for post-stroke depression, including both pharmacological and non-pharmacological approaches. In this review, we present evidence regarding the underlying biology of post-stroke depression, commonalities between post-stroke depression and Major Depressive Disorder and explore several treatment approaches, including antidepressant therapy, psychotherapy, surgical therapy, electroconvulsive therapy, acupuncture, music therapy and natural products. Further experimental and clinical studies are required, particularly in emerging fields such as the role of nutraceuticals in the treatment of stroke.

Stroke is an important cerebrovascular disease which causes chronic disability and death in patients. Despite of its high morbidity and mortality, there are limited available effective neuroprotective agents for stroke. In recent years, the research aimed at finding novel neuroprotective agents from natural origins has been intensified. Camellia sinensis L. (tea) is the second most consumed beverage worldwide, after water. It is classified into green and white, oolong, black and red, and Pu-erh tea based on the manufacturing process. Catechins are the main phytochemical constituents of Camellia sinensis which are known for their high antioxidant capacity. On other hand, it is well known that oxidative stress plays an important role in the initiation and progression of different cardiovascular diseases such as stroke. Therefore, the present article is aimed to review scientific studies that show the protective effects of tea consumption against ischemic stroke.

In the present study, three bi-3-azaoxoisoaporphine derivatives were synthesized and intracerebroventricularly administrated to BALB/c mice. The antidepressant actions in stroke-induced depressive like behavior in mice were examined using despair swimming test and tail suspension test. The results reported that bilateral common carotid arteries occlusion caused a significant abnormality of the normal behaviors. Behavioral models demonstrated that synthesized compounds showed antidepressant action. The most antidepressant active compound was DIME2 (4,4'-dimethyl-7H,7'H- [6,6'-bibenzo[e]perimidine]-7,7'-dione), which decreased the immobility time and increased the swimming and climbing times in despair swimming model. DIME2 also showed similar results in decreasing the immobility time in the tail suspension model. In open field tests, DIME2 at 0.1 μg/μl showed a significant activity in the modification of the distance movement and the number and duration of rearing versus bilateral common carotid arteries occlusion (P<0.001). Furthermore, bilateral common carotid arteries occlusion caused a significant increase in the water consumption and significant decreasing in the sucrose consumption which are indicated as a state of anhedonia, a well known common symptom of transient ischemic stroke-induced depressive like behavior, versus normal group (P<0.001). In conclusion, bi- 3-azaoxoisoaporphine derivatives can be considered as antidepressant agents for post stroke-induced depressive like behavior therapy.

In this study, antidepressant-like effects of intra-cerebroventricularly administration of oxoisoaporphine derivatives in post stroke-depressive like behavior were examined through despair swimming and tail suspension models. For this aim, acute ischemic stroke was induced by bilateral common carotid arteries occlusion which significantly changed the normal behaviors of male balb/c mice. We performed stroke-induced anhedonia test as a key result of post strokedepressive like behavior by determination of sucrose consumption. Results show that some 2,3-dihydro- and oxoisoaporphine derivatives modified the abnormality in the behaviors through decreasing in the immobility time in tail suspension and despair swimming models and increasing in the swimming and climbing times in despair swimming model. We concluded that these alkaloids showed antidepressant actions and therefore can be used for treatment of post strokedepressive like behavior in acute ischemic stroke patients.