Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies have illustrated that fatty acids, especially polyunsaturated fatty acids (PUFA), have a role in regulating oxidative stress via the enhancement of antioxidative defense capacity or the augmentation of oxidative burden. Elevated oxidative stress has been implicated in the pathogenesis of brain injury associated with cerebral ischemia/reperfusion (I/R). The objective of this study was to assess whether treatment with fatty acids after focal cerebral I/R induced by occlusion of the common carotid arteries and the middle cerebral artery has effects on brain injury in a rat model. PUFA, including arachidonic acid (AA) and docosahexaenoic acid (DHA), and the saturated fatty acid, stearic acid (SA), were administrated 60 min after reperfusion via intraperitoneal injection. AA and DHA aggravated cerebral ischemic injury, which manifested as enlargement of areas of cerebral infarction and increased impairment of motor activity, in a concentration-dependent manner. However, there were no remarkable differences in post-ischemic alterations between the SA and saline groups. The post-ischemic augmentation of injury in AA and DHA treatment groups was accompanied by increases in the permeability of the blood-brain barrier (BBB), brain edema, metalloproteinase (MMP) activity, inflammatory cell infiltration, cyclooxygenase 2 (COX-2) expression, caspase 3 activity, and malondialdehyde (MDA) production, and by a decrease in the brain glutathione (GSH) content. Furthermore, we found that either AA or DHA alone had little effect on free radical generation in neuroglia, but they greatly increased the hydrogen peroxide-induced oxidative burden. Taken together, these findings demonstrate the detrimental effect of PUFA such as AA and DHA in post-ischemic progression and brain injury after cerebral I/R is associated with augmentation of cerebral I/R-induced alterations, including oxidative changes.
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PMID:Detrimental effects of post-treatment with fatty acids on brain injury in ischemic rats. 1785 1

To determine whether Toxoplasma gondii infection could modify biological phenomena associated with brain ischemia, we investigated the effect of permanent middle cerebral artery occlusion (MCAO) on neuronal survival, inflammation and redox state in chronically infected mice. Infected animals showed a 40% to 50% decrease of infarct size compared with non-infected littermates 1, 4 and 14 days after MCAO. The resistance of infected mice may be associated with increased basal levels of anti-inflammatory cytokines and/or a marked reduction of the MCAO-related brain induction of two pro-inflammatory cytokines, tumor necrosis factor-alpha and interferon-gamma (IFNgamma). In addition, potential anti-inflammatory/neuroprotective factors such as nerve growth factor, suppressor of cytokine signaling-3, superoxide dismutase activity, uncoupling protein-2 and glutathione (GSH) were upregulated in the brain of infected mice. Consistent with a role of GSH in central cytokine regulation, GSH depletion by diethyl maleate inhibited Toxoplasma gondii lesion resistance by increasing the proinflammatory cytokine IFNgamma brain levels. Overall, these findings indicate that chronic toxoplasmosis decisively influences both the inflammatory molecular events and outcome of cerebral ischemia.
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PMID:Decreased infarct size after focal cerebral ischemia in mice chronically infected with Toxoplasma gondii. 1800 39

In dyscirculatory encephalopathy and moderate ischemic stroke there are single changes of components of glutathione metabolism. In moderate and severe ischemic stroke frequent and considerable changes have been revealed. Changes in hemorrhagic stroke are also expressed. An increase of activities of glutathione peroxidase and glutathione transferase is the most typical, rarely the increase of glutathione reductase and GSH is observed. The increase of enzymes activity was absent at the delayed oneset of treatment (more than 3 days) and in severe cases patients who died later. Glutathione system is important in the tolerance to cerebral ischemia.
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PMID:[Glutathione system in erythrocytes and blood plasma in strokes and dyscirculatory encephalopathy]. 1803 26

Stroke is a life-threatening disease characterized by rapidly developing clinical signs of focal or global disturbance of cerebral function due to cerebral ischemia. A number of flavonoids have been shown to attenuate the cerebral injuries in stroked animal models. Glabridin, a major flavonoid of Glycyrrhiza glabra (licorice), possesses multiple pharmacological activities. This study aimed to investigate whether glabridin modulated the cerebral injuries induced by middle cerebral artery occlusion (MCAO) in rats and staurosporine-induced damage in cultured rat cortical neurons and the possible mechanisms involved. Our study showed that glabridin at 25mg/kg by intraperitoneal injection, but not at 5mg/kg, significantly decreased the focal infarct volume, cerebral histological damage and apoptosis in MCAO rats compared to sham-operated rats. Glabridin significantly attenuated the level of brain malonyldialdehyde (MDA) in MCAO rats, while it elevated the level of two endogenous antioxidants in the brain, i.e. superoxide dismutase (SOD) and reduced glutathione (GSH). Co-treatment with glabridin significantly inhibited the staurosporine-induced cytotoxicity and apoptosis of cultured rat cortical neurons in a concentration-dependent manner. Consistently, glabridin significantly reduced the DNA laddering caused by staurosporine in a concentration-dependent manner. Glabridin also suppressed the elevated Bax protein and caspase-3 proenzyme and decreased bcl-2 induced by staurosporine in cultured rat cortical neurons, facilitating cell survival. Glabridin also inhibited superoxide production in cultured cortical neurons exposed to staurosporine. These findings indicated that glabridin had a neuroprotective effect via modulation of multiple pathways associated with apoptosis. Further studies are warranted to further investigate the biochemical mechanisms for the protective effect of glabridin on neurons and the evidence for clinical use of licorice in the management of cerebral ischemia.
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PMID:In vitro and in vivo neuroprotective effect and mechanisms of glabridin, a major active isoflavan from Glycyrrhiza glabra (licorice). 1804 62

The protective effects of in vitro cultivated calculus bovis (ICCB) on the cerebral and myocardial cells in hypoxic mice and the mechanism were examined. In one group, mice were intragastrically (i.g.) given ICCB for 15 days and then they were subjected to acute cerebral ischemia by decapitation, and then the panting time was recorded. In the other group, 12 min after exposure to hypoxia, mice was administered the ICCB i.g. for 5 days, and then the blood serum and tissues of brain, heart, liver were harvested and examined for SOD, GSH-px and T-AOC activity and content of MDA. The tissues of brain and heart were observed electron-microscopically for ultrastructural changes. The corpus striatum and hippocampus of brain were collected and examined for content of dopamine (DA) and norepinephrine (NE). The ultrastructural examination showed that the pathological change in brain and heart in the ICCB group was very slight, while abnormal changes in the control group were obviously more serious. ICCB significantly prolonged the panting time of the hypoxic mice (P<0.001), increased the activity of SOD, GSH-px, T-AOC in serum and tissues of brain, liver, heart and elevated the content of DA and NE. ICCB also pronouncedly reduced content of MDA in serum and tissues of brain, heart and liver. Significant differences in these parameters were noted between ICCB group and controls. It is concluded that ICCB can exert protective effect on the cells of brain and myocardium by enhancing the tolerance of the tissues to hypoxia and the body's ability to remove free radicals and regulating the neurotransmitters.
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PMID:The protective effects of in vitro cultivated calculus bovis on the cerebral and myocardial cells in hypoxic mice. 1823 29

The present study was conducted to investigate whether caffeic acid phenethyl ester (CAPE), an active component of propolis extract, has a protective effect on brain injury after focal permanent cerebral ischemia, and to determine the possible antioxidant mechanisms. Cerebral infarction in adult male New Zealand rabbits was induced by microsurgical procedures producing right focal permanent middle cerebral artery occlusion (pMCAO). CAPE was administered to the treatment group after pMCAO at a dose of 10 micromol kg(-1) once a day intraperitoneally for 7 days. Neurological deficits were evaluated, using a modified six-point scale. Spectrophotometric assay was used to determine the contents of malondialdehyde (MDA), glutathione (GSH), catalase (CAT), nitric oxide (NO) and xanthine oxidase (XO). In the ipsilateral hemisphere, the infarct volume of the brain was assessed in brain slices stained with heamatoxylen and eosin. The results showed that treatment with CAPE significantly reduced the percentage of infarction in the ipsilateral hemisphere compared with the ischemia group. CAPE treatment significantly attenuated the elevation of plasma MDA, CAT and XO content (p<0.05), whereas it significantly increased the levels of plasma GSH and NO (p<0.05). Therefore, subacute CAPE administration plays a protective role in focal pMCAO due to attenuation of lipid peroxidation and its antioxidant activity. All of these findings suggest that CAPE provides neuroprotection against cerebral ischemia injury through its antioxidant action.
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PMID:Caffeic acid phenethyl ester protects rabbit brains against permanent focal ischemia by antioxidant action: a biochemical and planimetric study. 1830 95

This study was to investigate the protective effects and possible mechanisms of total flavones of rhododendra (TFR) against cerebral ischemia reperfusion injury in rats and mice. Cerebral ischemia/reperfusion injury was induced by occluding the right middle cerebral artery (MCA). Infarct volume, neurological deficit, brain water content, levels of malondialdehyde (MDA), nitric oxide (NO) contents, lactate dehydrogenase (LDH) activity in plasma and brain, levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and mRNA expression of inducible nitric oxide synthase (iNOS), neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS) in brain were evaluated 7 or 10 days after treatment. TFR significantly reduced infarct volume, ameliorated the neurological deficit and reduced the brain water content. The activities of SOD, LDH and GPX in brain were enhanced, while the activity of LDH in plasma and the contents of MDA and NO in plasma and brain were decreased. While, the expression of iNOS and nNOS mRNA in brain were down-regulated, the expression of eNOS mRNA in the brain was up-regulated. These results suggest that TFR has protective effects for cerebral injury in rats and mice, which might be associated with its antioxidant properties and ability to regulate the expression of NOS isoforms.
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PMID:Protective effects of total flavones of rhododendra on cerebral ischemia reperfusion injury. 1845 65

Antioxidants have been the focus of studies for developing neuroprotective agents to be used in the therapy for stroke, which is an acute and progressive neurodegenerative disorder and is the second leading cause of death throughout the world. In fact, many herbal antioxidants have been developed in in vitro and in vivo experiments and some of these have been tested in clinical studies of stroke. Embelia ribes have been reported to have antioxidant and antidiabetic effects. In addition to these effects, this study was designed to investigate the neuroprotective effect of ethanolic extract of E. ribes Burm fruits on middle cerebral artery occlusion (MCAO)-induced focal cerebral ischemia in rats. Male Wistar albino rats were fed ethanolic E. ribes extract (100 and 200 mg/kg body weight; p.o.) for 30 days. After 30 days of feeding, all animals were anaesthetized with chloral hydrate (400 mg/kg, i.p.). The right middle cerebral artery was occluded with a 4-0 suture for 2 h. The suture was removed after 2 h to allow reperfusion injury. Ischemia followed by reperfusion in ischemic group rats significantly (P < 0.001) reduced the grip strength activity and non-enzymatic (reduced glutathione, GSH) and enzymatic [glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST)] antioxidant levels in hippocampus and frontal cortex compared to sham-operated rats. Further, serum lactate dehydrogenase (LDH) and thiobarbituric acid reactive substance (TBARS) levels in hippocampus and frontal cortex were significantly increased in ischemic group compared to sham-operated rats. Furthermore, ethanolic E. ribes extracts pretreatment significantly (P < 0.001) increased the grip strength activity, and GSH, GPx, GR and GST levels in hippocampus and frontal cortex with significant decrease in LDH levels in serum and TBARS levels in hippocampus and frontal cortex compared to MCAO + vehicle group rats. The data from this study suggest that chronic treatment with ethanolic E. ribes extract enhances the antioxidant defense against MCAO- induced focal cerebral ischemia in rats and exhibits neuroprotective activity.
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PMID:Evaluation of antioxidant and neuroprotective effect of ethanolic extract of Embelia ribes Burm in focal cerebral ischemia/reperfusion-induced oxidative stress in rats. 1848 49

Oxidative stress is implicated in the pathogenesis of cerebral ischemia injury, and the flavonoids have shown to be neuroprotective in experimental models of cerebral ischemia. Previously, we have shown that an aqueous preparation of quercetin did not reach the brain while a liposomal preparation produced measurable cerebral amounts of quercetin that reduced significantly the cerebral damage provoked by permanent middle cerebral artery occlusion (pMCAo) of rats. In this context, the protective effects of liposomal quercetin (LQ) were investigated in the same model after 1 and 4 hours of arterial occlusion. LQ was administered in a single dose (30 mg/kg), at 30 min, 1 and 4 h after pMCAo, and the brain was studied 24 h later. Cerebral damage and the oedema volume were assessed with a tetrazolium salt (TTC). The status of brain tissue, the neuronal population, the global motor behaviour as well as the antioxidant, endogenous reduced glutathione (GSH), were also assessed in the brain. Thirty min after LQ there was a significantly protective effect against ischemic lesion demonstrated by a significant increase in numbers of cells in striatum and cortex, together with a partial reversal of motor deficits. GSH levels decreased after ischemia in ipsilateral striatum and cortex, and the LQ preparation reversed these effects 24 h after the occlusion. Our results suggest that endogenous brain GSH is critical in the defense mechanisms after ischemia, as a significant mediator of the protective effects of the LQ preparation.
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PMID:Reduction of ischemic brain damage and increase of glutathione by a liposomal preparation of quercetin in permanent focal ischemia in rats. 1851 13

Extract of danshen (Salvia miltiorrhiza Bunge.) has been clinically prescribed in China to treat patients with stroke. The novel compound designated ND-309, namely isopropyl-beta-(3,4-dihydroxyphenyl)-alpha-hydroxypropanoate is a new metabolite of danshen in rat brain. The present study was conducted to investigate whether ND-309 has a protective effect on brain injury after focal cerebral ischemia, and to determine the possible mechanism. Adult male SD rats were subjected to middle cerebral artery occlusion (MCAO) by bipolar electro-coagulation. Behavioral tests were used to evaluate the damage to central nervous system. The cerebral infarct volume and edema were assessed to evaluate the brain patho-physiological changes. Spectrophotometric or spectrofluorometric assay methods were used to determine the generation of reactive oxygen species (ROS), activities of superoxide dismutase (SOD) and glutathione-peroxidase (GSH-Px), contents of malondialdehyde (MDA) and adenosine triphosphate (ATP), as well as respiratory control ratio of the brain mitochondria. The results showed that treatment with ND-309 significantly decreased neurological deficit scores, reduced infarct volume and the edema compared with the model group. Meanwhile, ND-309 significantly increased the brain ATP content, improved mitochondrial energy metabolism, attenuated the elevation of MDA content, the decrease in SOD, GSH-Px activity and the generation of ROS in brain mitochondria. All of these findings indicate that ND-309 has the protective potential against cerebral ischemia injury and its protective effects may be due to the amelioration of cerebral energy metabolism and its antioxidant property.
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PMID:ND-309, a novel compound, ameliorates cerebral infarction in rats by antioxidant action. 1865 75


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