Source:http://linkedlifedata.com/resource/pubmed/id/11675035
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| Predicate | Object |
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| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2001-10-24
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| pubmed:abstractText |
Free radicals have been implicated in neuronal injury during ischemia reperfusion in stroke. Therefore, in the present study, melatonin, a potent antioxidant, was studied in male Wistar rats subjected to 2 h of transient middle cerebral artery occlusion. Melatonin (10, 20 and 40 mg/kg i.p.) was administered four times in an animal at the time of middle cerebral artery occlusion, 1 h after middle cerebral artery occlusion, at the time of reperfusion and 1 h after reperfusion. Two hours after reperfusion, rats were euthanized for estimation of oxidative stress markers (malondialdehyde and reduced glutathione). The doses of 20 and 40 mg/kg of melatonin significantly attenuated the raised level of malondialdehyde (287+/-28, 279+/-52 nmol/g wet tissue, respectively) as compared to the levels (420+/-61 nmol/g wet tissue) in vehicle-treated middle cerebral artery-occluded rats. There was an insignificant change in levels of reduced glutathione at these doses (95+/-42, 88.7+/-36 microg/g wet tissue, respectively) as compared to those in the vehicle-treated middle cerebral artery-occluded rats (108.21+/-21 microg/g wet tissue). However, there was an insignificant difference between 20 and 40 mg/kg treated rats. Therefore, the dose of 20 mg/kg i.p. was used to evaluate the neuroprotective effect by using diffusion-weighted imaging (30 min after reperfusion), assessing the neurological deficit (24 h after middle cerebral artery occlusion) and estimating oxidative stress markers (72 h after middle cerebral artery occlusion). In the 20 mg/kg melatonin-treated group, percent ischemic lesion volume on diffusion-weighted imaging was significantly attenuated (9.8+/-3.9) as compared to that in the vehicle-treated group (21.4+/-4.7). The neurological deficit was significantly improved in the melatonin group (1.8+/-0.06) as compared to that in the vehicle-treated (2.9+/-0.38) group. The level of malondialdehyde (321.4+/-31 nmol/g wet tissue) and reduced glutathione (142.6+/-13 microg/g wet tissue) in the melatonin-treated group was also significantly decreased as compared to the level of malondialdehyde (623+/-22 nmol/g wet tissue) and reduced glutathione (226.6+/-19 microg/wet tissue) in the vehicle-treated group. The present study indicates that melatonin has a neuroprotective action in focal ischemia, which may be attributed to its antioxidant property.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0014-2999
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
5
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| pubmed:volume |
428
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
185-92
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| pubmed:dateRevised |
2003-11-14
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| pubmed:meshHeading |
pubmed-meshheading:11675035-Animals,
pubmed-meshheading:11675035-Antioxidants,
pubmed-meshheading:11675035-Brain,
pubmed-meshheading:11675035-Brain Ischemia,
pubmed-meshheading:11675035-Glutathione,
pubmed-meshheading:11675035-Infarction, Middle Cerebral Artery,
pubmed-meshheading:11675035-Injections, Intraperitoneal,
pubmed-meshheading:11675035-Magnetic Resonance Imaging,
pubmed-meshheading:11675035-Male,
pubmed-meshheading:11675035-Malondialdehyde,
pubmed-meshheading:11675035-Melatonin,
pubmed-meshheading:11675035-Rats,
pubmed-meshheading:11675035-Rats, Wistar,
pubmed-meshheading:11675035-Reperfusion Injury,
pubmed-meshheading:11675035-Survival Rate,
pubmed-meshheading:11675035-Time Factors
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| pubmed:year |
2001
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| pubmed:articleTitle |
Effect of melatonin on ischemia reperfusion injury induced by middle cerebral artery occlusion in rats.
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| pubmed:affiliation |
Department of Pharmacology, All India Institute of Medical Sciences, New Delhi-110029, India.
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| pubmed:publicationType |
Journal Article
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