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Conference Paper: The protective role of melatonin in rat hippocampal injuries induced by intermittent hypoxia

TitleThe protective role of melatonin in rat hippocampal injuries induced by intermittent hypoxia
Authors
Issue Date2007
PublisherFederation of American Societies for Experimental Biology.
Citation
The 2007 Annual Meeting of Experimental Biology (EB 2007), Washington, DC., 28 April–5 May 2007. In The FASEB Journal, 2007, v. 21 n. 6, p. A824 How to Cite?
AbstractWe evaluated the hypothesis that melatonin reduces hippocampal injuries with an increased expression of antioxidant enzymes during intermittent hypoxia (IH). Adult Sprague-Dawley rats received daily injection of melatonin or vehicle for 7 (D7), 14 (D14) and 28 days (D28) in IH chambers for 8 hr/day diurnally. Serum and hippocampus were harvested for the measurement of malondialdehyde (MDA). The mRNA levels of inflammatory mediators including TNFα, iNOS, COX-2 and antioxidant enzymes including glutathione peroxidase, catalase, copper/zinc superoxide dismutase in the hippocampus were studied by RT-PCR. Apoptosis was studied histologically in hippocampal sections. Our results showed significant increases in the cell death, levels of serum and hippocampal MDA and mRNA levels of inflammatory mediators in vehicle groups compared with the normoxic control, but mRNA levels of the antioxidant enzymes were decreased in those groups. The serum MDA level of melatonin groups was comparable to that of the normoxic control. Melatonin groups showed reduction in hippocampal MDA level and apoptosis compared with vehicle groups. Melatonin groups on D7 and D14 showed decreased expression of those mediators with elevated expressions of antioxidant enzymes compared with vehicle groups. However, melatonin had no effect on the expressions in inflammatory mediators or antioxidant enzymes on D28. These results suggest that melatonin reduces oxidative stress and delays the pathogenesis of IH-induced hippocampal injuries with its anti-oxidant and anti-inflammatory properties via transcriptional regulation of antioxidant enzymes. The transcriptional regulation may explain the protective effect against apoptosis in the early days of IH exposure.
Persistent Identifierhttp://hdl.handle.net/10722/95445
ISSN
2023 Impact Factor: 4.4
2023 SCImago Journal Rankings: 1.412

 

DC FieldValueLanguage
dc.contributor.authorHung, MWen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorPoon, AMSen_HK
dc.contributor.authorShiu, SYWen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-25T16:02:29Z-
dc.date.available2010-09-25T16:02:29Z-
dc.date.issued2007en_HK
dc.identifier.citationThe 2007 Annual Meeting of Experimental Biology (EB 2007), Washington, DC., 28 April–5 May 2007. In The FASEB Journal, 2007, v. 21 n. 6, p. A824en_HK
dc.identifier.issn0892-6638en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95445-
dc.description.abstractWe evaluated the hypothesis that melatonin reduces hippocampal injuries with an increased expression of antioxidant enzymes during intermittent hypoxia (IH). Adult Sprague-Dawley rats received daily injection of melatonin or vehicle for 7 (D7), 14 (D14) and 28 days (D28) in IH chambers for 8 hr/day diurnally. Serum and hippocampus were harvested for the measurement of malondialdehyde (MDA). The mRNA levels of inflammatory mediators including TNFα, iNOS, COX-2 and antioxidant enzymes including glutathione peroxidase, catalase, copper/zinc superoxide dismutase in the hippocampus were studied by RT-PCR. Apoptosis was studied histologically in hippocampal sections. Our results showed significant increases in the cell death, levels of serum and hippocampal MDA and mRNA levels of inflammatory mediators in vehicle groups compared with the normoxic control, but mRNA levels of the antioxidant enzymes were decreased in those groups. The serum MDA level of melatonin groups was comparable to that of the normoxic control. Melatonin groups showed reduction in hippocampal MDA level and apoptosis compared with vehicle groups. Melatonin groups on D7 and D14 showed decreased expression of those mediators with elevated expressions of antioxidant enzymes compared with vehicle groups. However, melatonin had no effect on the expressions in inflammatory mediators or antioxidant enzymes on D28. These results suggest that melatonin reduces oxidative stress and delays the pathogenesis of IH-induced hippocampal injuries with its anti-oxidant and anti-inflammatory properties via transcriptional regulation of antioxidant enzymes. The transcriptional regulation may explain the protective effect against apoptosis in the early days of IH exposure.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology.en_HK
dc.relation.ispartofThe FASEB Journalen_HK
dc.titleThe protective role of melatonin in rat hippocampal injuries induced by intermittent hypoxiaen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0892-6638&volume=21&issue=6&spage=733.11&epage=&date=2007&atitle=The+protective+effect+of+melatonin+on+hippocampal+injury+of+rats+in+intermittent+hypoxiaen_HK
dc.identifier.emailHung, MW: philiphung928@hotmail.comen_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailPoon, AMS: amspoon@hkucc.hku.hken_HK
dc.identifier.emailShiu, SYW: sywshiu@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.authorityShiu, SYW=rp00384en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.identifier.hkuros128921en_HK
dc.identifier.volume21en_HK
dc.identifier.issue6en_HK
dc.identifier.spageA824en_HK
dc.identifier.epageA824-
dc.identifier.issnl0892-6638-

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