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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of chloroform: methanolic (80:20) extract of C. asiatica (CA; 100 and 200 mg/kg), was evaluated on the course of free radical generation and excitotoxicity in monosodiumglutamate (MSG) treated female Sprague Dawley rats. The extract showed significant improvement in catalase, super oxide desmutase and lipid peroxides levels in hippocampus and striatum regions. Glutathione level was not altered with CA treatment. Similar observation was made with dextromethorphan. The general behavior, locomotor activity and CAl a region of the hippocampus was significantly protected by CA indicating neuroprotective effect of CA in MSG induced excitotoxic condition. Hence it can be concluded that CA protected MSG induced neurodegeneration attributed to its antioxidant and behavioural properties. This activity of CA can be explored in epilepsy, stroke and other degenerative conditions in which the role of glutamate is known to play vital role in the pathogenesis.
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PMID:Neuroprotective evaluation of standardized extract of Centella asciatica in monosodium glutamate treated rats. 1756 83

The generation of free radicals is a cause of many pathological conditions like diabetes mellitus, cancer, stroke, etc. Free radicals cause damage to cellular DNA and initiate carcinogenesis. Free radicals also bring about proliferation of cells via cell signaling. An inverse relationship between the consumption of vegetable diets and the risk of cancer has been established. In the present study, Star anise (Illicium verum), which is a commonly used condiment in Indian cuisine, was assessed for its anti-carcinogenic potential in N-nitrosodiethylamine (NDEA) initiated and phenobarbital (PB) promoted hepato-carcinogenesis. Rats were randomly selected for eight experimental groups. The carcinogenesis was induced by injecting the rats, with a single dose of NDEA (200mg/kg body weight) intraperitoneally as initiator, followed by promotion with PB (0.05%) in drinking water for 14 consecutive weeks. The treatment with NDEA increased liver weight, while Star anise (Star) treatment reduced the liver weight of rats. The treatment with Star throughout for 20 weeks or during the promotion stage (6-20 weeks) significantly reduced the nodule incidence and nodule multiplicity in the rats, while the treatment with Star at the initiation phase (first 4 weeks) only could not reduce these parameters. The treatment with Star for 20 consecutive weeks significantly reduced the nodule size and nodule volume. The treatment with Star throughout as well as at the promotion stage lowered the lipid peroxidation (LPO) in liver and erythrocytes, while the LPO was not lowered, when Star was administered during initiation stage only. The treatment with Star restored the liver and erythrocyte super-oxide dismutase (SOD) activities to normal in the carcinogenesis-induced rats. The liver catalase (CAT) activity increased in all the treated groups. The erythrocyte CAT activity increased in the rats treated with Star during initiation and promotion stage only. The liver glutathione (GSH) level increased significantly in the groups treated with Star. The erythrocyte GSH level was lowered in the rats treated with NDEA and PB, however, Star treatment helped in increasing the erythrocyte GSH level to some extent. The liver and erythrocyte glutathione-S-transferase (GST) activity increased in all the groups treated with NDEA and PB. The treatment with Star decreased GST level significantly. These results indicate that the treatment with Star reduces the tumor burden, lowers oxidative stress and increases the level of phase II enzymes, which may contribute to its anti-carcinogenic potential.
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PMID:Chemo-preventive effect of Star anise in N-nitrosodiethylamine initiated and phenobarbital promoted hepato-carcinogenesis. 1765 3

So far, several treatment modalities have been attempted to brain protection in cases such as brain trauma, stroke or brain hemorrhage. However, a treatment method that the effect begins immediately and definitely helpful has not been discovered yet. In this study, we aimed to compare the effects of propofol and erythropoietin (Epo) on brain injury caused by oxidative stress and antioxidant properties of these agents after closed head injury (CHI) in rats. For this study, female Wistar Albino rats were divided into five groups: non-traumatic control group, trauma performed group CHI, trauma with propofol (100 mg/kg) intraperitoneally (i.p.), trauma with Epo (5000 U/kg) i.p. and trauma with propofol and Epo performed study groups. Twenty-four hours after CHI, rats were sacrificed and the brains were removed. Superoxide dismutase (SOD), catalase (CAT), xanthine oxidase (XO), nitric oxide (NO), and malondialdehyde (MDA) levels were measured in brain tissue. MDA and NO levels were decreased significantly in Groups Epo, Propofol and Epo+Propofol than Group CHI (p<0.01). XO activity was significantly lower in Group Epo than Group CHI (p<0.05). Epo and propofol decreased oxidative stress by decreasing MDA and NO level in brain tissue after CHI. However, combination of Epo and propofol has no significant beneficial advantage than Epo or propofol alone.
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PMID:Propofol and erythropoietin antioxidant properties in rat brain injured tissue. 1776 98

Emerging epidemiological data indicates that diabetes is a potential predisposing factor for neuropsychiatric deficits as stroke, cerebrovascular diseases, diabetic encephalopathy, depression and anxiety. Diabetic encephalopathy, characterized by impaired cognitive functions and neurochemical and structural abnormalities, involves direct neuronal damage caused by intracellular glucose. Curcumin, a well-established phenolic antioxidant and anti-inflammatory molecule, is capable of playing an important role against amyloid and dendritic pathology and thus has neuroprotective properties. The aim of the present study was to explore the effect of curcumin (60 mg/kg; p.o.) on cognitive functions, oxidative stress and inflammation in diabetic rats. Learning and memory behaviors were investigated using a spatial version of the Morris water maze test. Acetylcholinesterase activity, a marker of cholinergic dysfunction, was increased by 80% in the cerebral cortex of diabetic rats. There was 107% and 121% rise in thiobarbituric acid reactive substance levels in cerebral cortex and hippocampus of diabetic rats, respectively. Reduced glutathione level and enzymatic activities of superoxide dismutase and catalase were decreased in both cerebral cortex and hippocampal regions of diabetic rat brain. Nitrite levels in cerebral cortex and hippocampus were increased by 112% and 94% respectively. Serum TNF-alpha, a marker for inflammation, was found to increase by 1100% in diabetic rats. Chronic treatment with curcumin (60 mg/kg; p.o.) significantly attenuated cognitive deficit, cholinergic dysfunction, oxidative stress and inflammation in diabetic rats. The results emphasize the involvement of cholinergic dysfunction, oxidative stress and inflammation in the development of cognitive impairment in diabetic animals and point towards the potential of curcumin as an adjuvant therapy to conventional anti-hyperglycemic regimens for the prevention and treatment of diabetic encephalopathy.
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PMID:Curcumin attenuates diabetic encephalopathy in rats: behavioral and biochemical evidences. 1782 93

Emerging epidemiologic data indicates that diabetes is a potential predisposing factor for neuropsychiatric deficits as stroke, cerebrovascular diseases, diabetes-associated cognitive decline, depression and anxiety. Diabetes-associated cognitive decline, characterized by impaired cognitive functions and neurochemical and structural abnormalities, involves direct neuronal damage caused by intracellular glucose. The present study was designed to investigate the effect of sesamol (3,4-methylenedioxyphenol), a phenolic antioxidant and anti-inflammatory molecule, on cognitive functions, oxidative stress and inflammation in diabetic rats. Learning and memory behaviors were investigated using a spatial version of the Morris water maze test. Acetylcholinesterase activity, a marker of cholinergic dysfunction, was increased by 80% in the cerebral cortex of diabetic rats. There was 107 and 121% rise in thiobarbituric acid reactive substance levels in cerebral cortex and hippocampus of diabetic rats, respectively. Reduced glutathione levels and enzymatic activities of superoxide dismutase and catalase were decreased in both cerebral cortex and hippocampal regions of diabetic rat brain. Nitrite levels in cerebral cortex and hippocampus was increased by 138 and 109%, respectively. Serum tumor necrosis factor-alpha, a marker for inflammation, was found to increase by 1,100% in diabetic rats. Chronic treatment with sesamol (2, 4 and 8 mg/kg; p.o.) significantly and dose-dependently attenuated cognitive deficit, reduced acetylcholinesterase, oxidative stress and inflammation in diabetic rats. The results emphasize the involvement of oxidative stress and inflammation in the development of cognitive impairment in diabetic animals and point towards the therapeutic potential of sesamol in diabetes-associated cognitive decline.
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PMID:Effect of sesamol on diabetes-associated cognitive decline in rats. 1795 23

This review focuses on the morphological features of atherosclerosis and the involvement of oxidative stress in the initiation and progression of this disease. There is now consensus that atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein in the vascular wall. Reactive oxygen species (ROS) are key mediators of signaling pathways that underlie vascular inflammation in atherogenesis, starting from the initiation of fatty streak development, through lesion progression, to ultimate plaque rupture. Plaque rupture and thrombosis result in the acute clinical complications of myocardial infarction and stroke. Many data support the notion that ROS released from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, myeloperoxidase (MPO), xanthine oxidase (XO), lipoxygenase (LO), nitric oxide synthase (NOS) and enhanced ROS production from dysfunctional mitochondrial respiratory chain, indeed, have a causatory role in atherosclerosis and other vascular diseases. Moreover, oxidative modifications in the arterial wall can contribute to the arteriosclerosis when the balance between oxidants and antioxidants shifts in favour of the former. Therefore, it is important to consider sources of oxidants in the context of available antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase and transferases thiol-disulfide oxidoreductases and peroxiredoxins. Here, we review also the mechanisms in which they are involved in order to accelerate the pace of the discovery and facilitate development of novel therapeutic approaches.
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PMID:Atherosclerosis and oxidative stress. 1807 94

Oxidative stress, resulting from mitochondrial dysfunction, excitotoxicity, or neuroinflammation, is implicated in numerous neurodegenerative conditions. Damage due to superoxide, hydroxyl radical, and peroxynitrite has been observed in diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, as well as in acute conditions that lead to neuronal death, such as stroke and epilepsy. Antioxidant therapies to remove these toxic compounds have been of great interest in treating these disorders. Catalytic antioxidants mimic the activities of superoxide dismutase or catalase or both, detoxifying superoxide and hydrogen peroxide, and in some cases, peroxynitrite and other toxic species as well. Several compounds have demonstrated efficacy in in vitro and in animal models of neurodegeneration, leading to optimism that catalytic antioxidants may prove to be useful therapies in human disease.
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PMID:Catalytic antioxidants and neurodegeneration. 1875 9

The aim of the study--to estimate the effect of therapy with Magne 6 on the indices of cardiac hemodynamics, tolerance to physical load, activity of antioxidant protection enzymes and grade of hypoxia in youths with 1 grade mitral valve prolapse (MVP) without regurgitation. In 73 cases with impaired compensatory adaptive possibilities the extent of main syndromes of autonomic dystonia and state of cardiac hemodynamic indices were evaluated. The activity of catalase (C), glutathione reductase (GR), superoxide dismutase (SOD), lactate (L) and pyruvate (P) level were detected in red blood cells, the coefficient lactate/pyruvate (L/P) was been calculated according to the standard method. In the study the high-grade of autonomic dystonia (36.6 +/- 2.1 scores) was been revealed. The number of scores in the control group is 10.8 +/- 1.8. There was found the confident increase of stroke by 37.18%, cardiac output by 24%, stroke index--by 38.45% and cardiac index--by 43.06% in comparison with healthy persons (a < 0.05). The time of cycle ergometer load was significantly lower than in reference group 20.22% (a < 0.05). The red blood cells levels of PVK and L were correspondingly 95.4% and 51.4% higher than in control (p < 0.05). The L/P ratio was 22.5% in excess of the value in reference group (p < 0.05). C activity was 4.59 times less, SOD and GR activity were correspondingly 6.23 and 1.85 times (p < 0.05) as mush, than in healthy persons. Associated with Magne 6 therapy for a month the improvement in indices of cardiac hemodynamics, rising of tolerance to physical load, the fall in GR activity and decrease of hypoxia were been noted. Magne 6 may be used for magnifying of compensatory--adaptive possibilities in youths with 6 MVP.
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PMID:[The use of Magne B6 in order to increase compensatory-adaptive possibilities in youths with primary mitral valve prolapse]. 1875 51

No effective therapy is available for treating intracerebral hemorrhage (ICH). One of several key components of brain damage after ICH is the neurotoxicity of blood products. Within hours to days after ICH, extravasated erythrocytes in the hematoma undergo lysis, releasing cytotoxic hemoglobin, heme, and iron, thereby initiating secondary processes, which negatively influence the viability of cells surrounding the hematoma. To offset this process, phagocytic cells, including the brain's microglia and hematogenous macrophages, phagocytose and then process extravasated erythrocytes before lysis and subsequent toxicity occurs. Therefore, we hypothesize that a treatment that stimulates phagocytosis will lead to faster removal of blood from the ICH-affected brain, thus limiting/preventing hemolysis from occurring. CD36 is a well-recognized integral microglia/macrophage cell membrane protein known to mediate phagocytosis of damaged, apoptotic, or senescent cells, including erythrocytes. CD36 and catalase expression are regulated by peroxisome proliferator activated receptor-gamma agonists (eg, rosiglitazone). We demonstrate that peroxisome proliferator activated receptor-gamma agonist-induced upregulation of CD36 in macrophages enhances the ability of microglia to phagocytose red blood cells (in vitro assay), helps to improve hematoma resolution, and reduces ICH-induced deficit in a mouse model of ICH. The beneficial role of peroxisome proliferator activated receptor-gamma-induced catalase expression in the context of phagocytosis is also discussed. Proxisome proliferator activated receptor-gamma agonists could represent a potential treatment strategy for treatment of ICH.
Stroke 2009 Mar
PMID:Hematoma resolution as a therapeutic target: the role of microglia/macrophages. 1906 96

Free radicals are molecules or ions containing non-paired electrons on the external orbit, which ensures their high chemical activity. In systemic homeostasis, free radicals are inactivated by endo- and exogenous antioxidants and do not have destructive effects. The human organism possesses protective mechanisms, i.e. enzymatic systems (peroxide dismutase, glutathione peroxidase, catalase) and non-enzymatic systems (vitamin C and E selenium, coenzyme Q, lipoid acid, bilirubin). Imbalance between continuous production of reactive oxygen forms and their elimination due to enzymatic and non-enzymatic neutralization reactions as well as effects of exogenous antioxidants is defined as oxidative stress. Recent studies demonstrated a significant role of inflammatory processes and oxidative stress in the pathomechanism of cerebral stroke. Increased production of free radicals was observed in both the ischaemic and haemorrhagic strokes and oxidative stress was shown to be one of the causative mechanisms of tissue damage in these diseases. This was confirmed by numerous studies assessing the concentration of oxidative stress biomarkers and levels of plasma antioxidants (enzymatic and non-enzymatic). At present, studies are being carried out about the use of antioxidative substances for the therapy of cerebral stroke. The present study reports current findings concerning oxidative stress issues in patients with stroke.
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PMID:[Oxidative stress in cerebral stroke]. 1911 32


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