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)

The study was aimed at the investigation of the rat corticospinal system both functionally and anatomically using as a functional marker the immediate early gene c-fos, combined with retrograde tracing with horseradish peroxidase (HRP). This was achieved by mapping c-fos induction immunocytochemically in the spinal cord as a result of occlusion of the middle cerebral artery (MCA). Following left-sided MCA occlusion, Fos-like immunoreactivity (Fos-LI) was localized in both the dorsal and ventral horn neurons at the lumbar segment of the spinal cord. Labelling was often bilateral but was generally more substantial ipsilaterally. In the ventral horn, some of the Fos-positive neurons were confirmed to be somatic motoneurons innervating the tibialis anterior muscle of the lower extremity contralateral to MCA occlusion, as shown by their retrograde labelling with horseradish peroxidase injected into the muscle. Fos-LI was absent in the ventral horn of the spinal cord at cervical, thoracic, and sacral segments in both experimental and sham-operated rats. These findings suggest that the expression of c-fos may be used as a sensitive transneuronal marker for the study of neuronal activity in the spinal cord elicited by brain damage, viz. focal cerebral ischaemia, and when coupled with injection of HRP as a retrograde tracer, the method may prove to be useful for the study of transneuronal effect of the damage of the corticospinal motor system. While the expression of c-fos in the spinal motoneurons was most probably attributable to transneuronal effect following MCA occlusion, the possibility of that c-fos can be induced by altered hindlimb activity after the cerebral ischaemic insult cannot be excluded.
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PMID:Expression of Fos in the spinal motoneurons labelled by horseradish peroxidase following middle cerebral artery occlusion in rat. 956

Endothelial barrier antigen (EBA) can be used to detect the blood-brain barrier in the central nervous system of rats. This study investigated the temporal profile of antigen expression in cerebral vessels after infarction and assessed the relationship between re-establishment of this antigen in newly formed vessels and astrocytes around these vessels. Rats were subjected to cerebral ischemia for 2 h by the intraluminal thread method, then killed after 1, 3, 7, 14 and 28 days. Perfusion-fixed paraffin-embedded brains were immunostained for detection of EBA and glial fibrillary acidic protein (GFAP) by the streptavidin-biotin-peroxidase complex method. EBA immunostaining in vessels in the infarcted lesion was reduced at day 1 and had almost disappeared by day 3. Newly formed vessels were found from day 3, but were not stained at day 7. However, these new vessels were weakly stained at day 14 and definitely stained at day 28. GFAP immunostaining was completely negative around these proliferating vessels. The temporal profile of disappearance and re-expression of EBA in cerebral infarcted lesion may be associated with aggravation and improvement of brain edema, although barrier permeability was not explored in this study. The expression of this antigen has no relationship to the formation of astrocyte/endothelial contacts.
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PMID:Impairment and restoration of the endothelial blood-brain barrier in the rat cerebral infarction model assessed by expression of endothelial barrier antigen immunoreactivity. 1066 64

Stroke, or ischaemic brain damage, is of great geriatric importance being the third most common cause of death after cancer and heart diseases in developed countries. Despite such high frequency, its management has received inadequate attention. Many studies have shown the role of free radicals in the pathogenesis of ischaemic brain damage. Search for safe and effective antioxidant and free radial scavenger agents, therefore, appear to be a promising approach for stroke therapy. Gold, widely used in modern medicine for the treatment of rheumatoid arthritis, is highly valued for various medicinal uses in Indian systems of medicine. Traditional gold preparations are attributed with tonic/rejuvenating and antioxidant properties. Our earlier studies revealed interesting analgesic, immunostimulant, adaptogenic and glycogen sparing properties in these preparations, but their effects in cerebral ischaemia have not been investigated. This prompted us to initiate the present study using global and focal models of ischaemia in albino rats. Enzymatic parameters (lipid peroxidase, reduced glutathione, catalase, glutathione reductase, glutathione-S-transferase, glutatione peroxidase, superoxide dismutase, and glucose-6-phosphate dehydrogenase) were employed to assess ischaemic brain damage and its modulation. Significant restoration of altered values to near normal levels by Ayurvedic Swarna Bhasma and Unani Kushta Tila Kalan (25 mg/kg, orally for 10 days), suggest potentials for gold preparations in cerebrovascular diseases. The preparations deserve more scientific attention for possible therapeutic exploitation.
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PMID:Antioxidant/restorative effects of calcined gold preparations used in Indian systems of medicine against global and focal models of ischaemia. 1207 6

Reactive oxygen species produced by neutrophils contribute to the pathogenesis of focal cerebral ischemia/reperfusion injury and signal the inflammatory response. We have previously shown that honokiol, an active principle extracted from Magnolia officinalis, has a protective effect against focal cerebral ischemia/reperfusion injury in rats that paralleled a reduction in reactive oxygen species production by neutrophils. To elucidate the underlying mechanism(s) of the antioxidative effect of honokiol, peripheral neutrophils isolated from rats were activated with phorbol-12-myristate-13-acetate (PMA) or N-formyl-methionyl-leucyl-phenylalanine (fMLP) in the presence or absence of honokiol. In this study, we found that honokiol inhibited PMA- or fMLP-induced reactive oxygen species production by neutrophils by three distinct mechanisms: (1) honokiol diminished the activity of assembled-NADPH oxidase, a major reactive oxygen species producing enzyme in neutrophils by 40% without interfering with its protein kinase C (PKC)-dependent assembly; (2) two other important enzymes for reactive oxygen species generation in neutrophils, i.e., myeloperoxidase and cyclooxygenase, were also inhibited by honokiol by 20% and 70%, respectively; and (3) honokiol enhanced glutathione (GSH) peroxidase activity by 30%, an enzyme that triggers the metabolism of hydrogen peroxide (H2O2). These data suggested that honokiol, acting as a potent reactive oxygen species inhibitor/scavenger, could achieve its focal cerebral ischemia/reperfusion injury protective effect by modulating enzyme systems related to reactive oxygen species production or metabolism, including NADPH oxidase, myeloperoxidase, cyclooxygenase, and GSH peroxidase in neutrophils.
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PMID:The anti-inflammatory effect of honokiol on neutrophils: mechanisms in the inhibition of reactive oxygen species production. 1295 55

This study was conducted to investigate the neuroprotective effects of 20(S)-ginsenoside Rg3 on focal cerebral ischemia in rats. Middle cerebral artery occlusion (MCAO) model in male Wistar-Kyoto (WKY) rats was employed. The behavioral tests were used to evaluate the damage to central nervous system. The infarct area of brain was assessed in the brain slices stained with 2,3,5-triphenyltetrazolium chloride (TTC). Hydrogen clearance techniques were used to monitor regional cerebral blood flow (rCBF), spectrophotometric assay methods were used to determine the activities of superoxide dismutase (SOD) and glutathione-peroxidase (GSH-Px), contents of malondialdehyde (MDA) and adenosine triphosphate (ATP) of the brain. Furthermore, the respiratory control ratio (RCR=State 3/State 4) was assessed in the brain mitochondria. The results showed that sublingual vein injection of 20(S)-ginsenoside Rg3 at doses of 10 and 5 mg kg(-1), but not 2.5 mg kg(-1) exhibited significant neuroprotective effects on rats against focal cerebral ischemic injury by markedly decreasing neurological deficit scores, reducing the infarct area and enhancing the rCBF compared with the control group. At the same time, 20(S)-ginsenoside Rg3 significantly improved mitochondrial energy metabolism, antagonized decreases in SOD and GSH-Px activities and increase in MDA level induced by cerebral ischemia. All these findings suggest that 20(S)-ginsenoside Rg3 might provide neuroprotection against the cerebral ischemia-induced injury in rat brain through reducing lipid peroxides, scavenging free radicals and improving the energy metabolism.
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PMID:Neuroprotective effect of 20(S)-ginsenoside Rg3 on cerebral ischemia in rats. 1564 71

To investigate the protective effect of ginsenoside Re (Re) against cerebral ischemia-reperfusion injury, adult male Wistar rats weighing 250-300 g were subjected to either sham surgery or middle cerebral artery occlusion (MCAO) for 2 h of brain ischemia and 2 h reperfusion. A fluorescence polarization assay was carried out for membrane fluidity of brain mitochondria. Lipid peroxidation [malondiadehyde (MDA) formation], superoxide dismutase (SOD) and glutathion peroxidase (GSH-Px) of rat brain were estimated by fluorometric methods. It was observed that Re (5, 10, 20 mg kg-1 p.o. pretreatment for 7 d, once a day) significantly improved the fluidity of mitochondrial membranes as demonstrated by a reduction of average microviscosity, ameliorated lipid peroxidation by raising the activities of SOD and GSH-Px, and reduced the content of MDA in rat brain. This study demonstrated a direct protective effect of Re against cerebral ischemia-reperfusion injury.
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PMID:Protective effect of ginsenoside-Re against cerebral ischemia/reperfusion damage in rats. 1714 90

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

(2E)-2-{6-[(E)-2-carboxylvinyl]-2,3-dihydroxyphenyl}-3-(3,4-dihydroxyphenyl) propenoic acid, a novel compound designated SMND-309, is a new degradation product of salvianolic acid B. The present study was conducted to evaluate whether SMND-309 has a protective effect on permanent focal cerebral ischemia in rats. The results showed that SMND-309 at doses higher than 4.0 mg/kg (i.v.) produced a significant neuroprotection in focal ischemia rats when administered 30 min after the onset of ischemia. SMND-309 (25.0 mg/kg, i.v.) demonstrated significant neuroprotective activity even after delayed administration at 1 h, 3 h and 6 h after ischemia. The neuroprotective effect of SMND-309 (25.0 mg/kg, bolus injection intravenous at 30 min after middle cerebral artery occlusion) was still present 7 days after ischemia. Meanwhile, SMND-309 significantly increased the brain ATP content, improved mitochondrial energy metabolism and mitochondrial respiratory chain complex activities and attenuated the elevation of malondialdehyde (MDA) content, the decrease in superoxide dismutase (SOD) and glutathione-peroxidase (GSH-Px) activity in brain mitochondria. All of these findings indicate that SMND-309 exerts potent and long-term neuroprotective effects with a favorable therapeutic time-window in the model of permanent cerebral ischemia, and its protective effects may be due to the amelioration of cerebral mitochondrial energy metabolism and the antioxidant property.
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PMID:SMND-309, a novel derivate of salvianolic acid B, ameliorates cerebral infarction in rats: characterization and role. 1936 34

This study was conducted to investigate the efficacy of cornin, an iridoid glycoside, in an experimental cerebral ischemia induced by middle cerebral artery occlusion (MCAO) and reperfusion (I/R), and to elucidate the potential mechanism. Adult male Sprague-Dawley rats were subjected to MCAO for 1 h, then reperfusion for 23 h. Behavioral tests were used to evaluate the damage to central nervous system. The cerebral infarct volume and histopathological damage were assessed to evaluate the brain pathophysiological changes. Spectrophotometric assay methods were used to determine the activities of superoxide dismutase (SOD) and glutathione-peroxidase (GPx). Contents of malondialdehyde (MDA), the generation of reactive oxygen species (ROS) as well as respiratory control ratio and respiratory enzymes of the brain mitochondria were also determined. The results showed that cornin significantly decreased neurological deficit scores, and reduced cerebral infarct volume and degenerative neurons. Meanwhile, cornin significantly increased the brain ATP content, improved mitochondrial energy metabolism, inhibited the elevation of MDA content and ROS generation, and attenuated the decrease of SOD and GPx activities in brain mitochondria. These findings indicate that cornin has protective potential against cerebral ischemia injury and its protective effects may be due to amelioration of cerebral mitochondrial function and its antioxidant property.
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PMID:Cornin ameliorates cerebral infarction in rats by antioxidant action and stabilization of mitochondrial function. 2004 27

Our present study was conducted to investigate whether liquiritin (7-hydroxy-2-[4-[3,4,5-trihydroxy-6-(hydroxymethyl) oxan-2-yl] oxyphenyl]-chroman-4-one, 1), an active component of Glycyrrhiza uralensis Fisch., exerts a neuroprotective effect against focal cerebral ischemia/reperfusion (I/R) in male Institute of Cancer Research (ICR) mice. On the establishment of mice with middle cerebral artery occlusion (MCAO) for 2 h and reperfusion for 22 h, liquiritin at the doses of 40, 20, and 10 mg/kg was administered before MCAO once a day intragastrically for a subsequent 3 days. Neurological deficits and infarct volume were measured, respectively. The levels of malondialdehyde (MDA) and carbonyl, activities of superoxide anion (SOD), catalase (CAT) and glutathion peroxidase (GSH-Px) and reduced glutathione/oxidized disulfide (GSH/GSSG) ratio in brain were estimated spectrophotometrically. 8-Hydroxy-2'-deoxyguanosine (8-OHdG) and terminal deoxynucleotidyl transferase-mediated DuTP-biotin nick end labeling (TUNEL)-positive cells were detected by immunohistochemical analysis. Our results showed that the neurological deficits, infarct volume, and the levels of MDA and carbonyl decreased, the ratio of GSH/GSSG and the activities of SOD, CAT, and GSH-Px were compensatorily up-regulated, and 8-OHdG and TUNEL-positive cells decreased after 22 h of reperfusion in liquiritin-treated groups. These findings suggest that liquiritin might be a potential agent against cerebral I/R injury in mice by its antioxidant and antiapoptosis properties.
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PMID:Neuroprotective effect of liquiritin against focal cerebral ischemia/reperfusion in mice via its antioxidant and antiapoptosis properties. 2112 46


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