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Article: Protective effect of melatonin against hippocampal injury of rats with intermittent hypoxia

TitleProtective effect of melatonin against hippocampal injury of rats with intermittent hypoxia
Authors
KeywordsAntioxidant enzymes
Apoptosis
Inflammation
Intermittent hypoxia
Melatonin
Issue Date2008
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPI
Citation
Journal Of Pineal Research, 2008, v. 44 n. 2, p. 214-221 How to Cite?
AbstractObstructive sleep apnea (OSA) patients suffer from intermittent hypoxia (IH) and neuropsychologic impairments. Oxidative stress is involved in the pathogenesis of OSA, so the application of an antioxidant may be useful. We evaluated the hypothesis that melatonin would reduce IH-induced hippocampal injury via an increased expression of antioxidant enzymes. Adult Sprague-Dawley rats that had received a daily injection of melatonin or vehicle were exposed to IH for 8 hr/day for 7 or 14 days. The serum and hippocampus were harvested for the measurement of malondialdehyde (MDA). Apoptotic cell death was studied histologically in hippocampal sections. The mRNA expression of inflammatory mediators including tumor necrosis factor-alpha, inducible nitric oxide synthase, cyclooxygenase-2 and antioxidant enzymes including glutathione peroxidase, catalase and copper/zinc superoxide dismutase were examined in the hippocampus by RT-PCR. The results show significant increases in levels of serum and hippocampal MDA, apoptotic cell death and mRNA levels of inflammatory mediators in hypoxic rats when compared with the normoxic controls. Also, mRNA levels of the antioxidant enzymes were decreased in hypoxic animals. In the melatonin-treated hypoxic rats, serum MDA levels were comparable with those in normoxic control rats. Also, melatonin treatment significantly reduced hippocampal MDA levels and totally prevented apoptosis. Moreover, there were a decreased expression of the inflammatory mediators and an elevated expression of antioxidant enzymes in the melatonin injected rats when compared with vehicle-treated animals. These results indicate that melatonin mitigates oxidative stress and the pathogenesis of IH-induced hippocampal injury via its antioxidant and anti-inflammatory properties which includes stimulation of transcriptional regulation of antioxidant enzymes. © 2007 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/67415
ISSN
2015 Impact Factor: 9.314
2015 SCImago Journal Rankings: 2.655
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHung, MWen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorPoon, AMSen_HK
dc.contributor.authorReiter, RJen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-06T05:54:56Z-
dc.date.available2010-09-06T05:54:56Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Pineal Research, 2008, v. 44 n. 2, p. 214-221en_HK
dc.identifier.issn0742-3098en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67415-
dc.description.abstractObstructive sleep apnea (OSA) patients suffer from intermittent hypoxia (IH) and neuropsychologic impairments. Oxidative stress is involved in the pathogenesis of OSA, so the application of an antioxidant may be useful. We evaluated the hypothesis that melatonin would reduce IH-induced hippocampal injury via an increased expression of antioxidant enzymes. Adult Sprague-Dawley rats that had received a daily injection of melatonin or vehicle were exposed to IH for 8 hr/day for 7 or 14 days. The serum and hippocampus were harvested for the measurement of malondialdehyde (MDA). Apoptotic cell death was studied histologically in hippocampal sections. The mRNA expression of inflammatory mediators including tumor necrosis factor-alpha, inducible nitric oxide synthase, cyclooxygenase-2 and antioxidant enzymes including glutathione peroxidase, catalase and copper/zinc superoxide dismutase were examined in the hippocampus by RT-PCR. The results show significant increases in levels of serum and hippocampal MDA, apoptotic cell death and mRNA levels of inflammatory mediators in hypoxic rats when compared with the normoxic controls. Also, mRNA levels of the antioxidant enzymes were decreased in hypoxic animals. In the melatonin-treated hypoxic rats, serum MDA levels were comparable with those in normoxic control rats. Also, melatonin treatment significantly reduced hippocampal MDA levels and totally prevented apoptosis. Moreover, there were a decreased expression of the inflammatory mediators and an elevated expression of antioxidant enzymes in the melatonin injected rats when compared with vehicle-treated animals. These results indicate that melatonin mitigates oxidative stress and the pathogenesis of IH-induced hippocampal injury via its antioxidant and anti-inflammatory properties which includes stimulation of transcriptional regulation of antioxidant enzymes. © 2007 The Authors.en_HK
dc.languageengen_HK
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPIen_HK
dc.relation.ispartofJournal of Pineal Researchen_HK
dc.subjectAntioxidant enzymesen_HK
dc.subjectApoptosisen_HK
dc.subjectInflammationen_HK
dc.subjectIntermittent hypoxiaen_HK
dc.subjectMelatoninen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnoxia - metabolism - pathology - prevention & controlen_HK
dc.subject.meshHippocampus - drug effects - metabolism - pathologyen_HK
dc.subject.meshInflammation Mediators - therapeutic useen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMelatonin - administration & dosage - therapeutic useen_HK
dc.subject.meshNeuroprotective Agents - administration & dosage - therapeutic useen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshTime Factorsen_HK
dc.titleProtective effect of melatonin against hippocampal injury of rats with intermittent hypoxiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0742-3098&volume=44&spage=214&epage=221&date=2008&atitle=Protective+effect+of+melatonin+against+hippocampal+injury+of+rats+with+intermittent+hypoxiaen_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailPoon, AMS: amspoon@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityPoon, AMS=rp00354en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1600-079X.2007.00514.xen_HK
dc.identifier.pmid18289174-
dc.identifier.scopuseid_2-s2.0-39149087649en_HK
dc.identifier.hkuros141235en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-39149087649&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume44en_HK
dc.identifier.issue2en_HK
dc.identifier.spage214en_HK
dc.identifier.epage221en_HK
dc.identifier.eissn1600-079X-
dc.identifier.isiWOS:000253257400014-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridHung, MW=16744402300en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridPoon, AMS=7103068868en_HK
dc.identifier.scopusauthoridReiter, RJ=7402574751en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.citeulike2389718-

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