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Article: Cigarette smoke-induced cerebral cortical interleukin-6 elevation is not mediated through oxidative stress

TitleCigarette smoke-induced cerebral cortical interleukin-6 elevation is not mediated through oxidative stress
Authors
KeywordsNeuroinflammation
Nitric oxide
Reactive oxygen species
Smoking
Issue Date2012
PublisherF P Graham Publishing Company. The Journal's web site is located at http://www.fpgrahamco.com/Neuro/index.html
Citation
Neurotoxicity Research, 2012, v. 22 n. 2, p. 170-176 How to Cite?
AbstractThe author group has previously established an in vivo subchronic cigarette smoke (CS) exposure rat model, in which the systemic oxidative burden as well as the modulation of local anti-oxidative enzymes in the lung has been demonstrated. Oxidative stress has been shown to induce pro-inflammatory cytokine release, including interleukin (IL)-6 in the airways. In this study, we aimed to investigate the changes in IL-6 production, as well as the oxidative/anti-oxidative responses in the cerebral cortex using the same in vivo model. IL-6 was determined by RT-PCR and western-blot analysis. Local oxidative and anti-oxidative responses were determined by measuring cerebral cortical malondialdehyde (MDA) and advanced oxidation protein product (AOPP) levels, superoxide dismutase (SOD) and catalase activities, and the reduced to oxidized glutathione (GSH/GSSG) ratio. Nitrite level was measured by fluorescent spectrophotometry. Our results demonstrated a significant increase in both IL-6 mRNA and protein levels. Reductions of SOD activity and manganese (Mn)SOD protein level were observed together with the increased level of superoxide measured by chemiluminescent signal, after 56 days of CS exposure. There were no significant changes in the cerebral cortical levels of MDA, AOPP, catalase activity, and the GSH/GSSG ratio. Nitrite level was significantly reduced, together with the decreased protein level of nNOS in the cerebral cortex, after 56 days of CS exposure. Our results suggest that exposure to CS induces IL-6 expression in the cerebral cortex, which is not mediated by the oxidative/anti-oxidative imbalance. © 2012 Springer Science+Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/147110
ISSN
2023 Impact Factor: 2.9
2023 SCImago Journal Rankings: 0.789
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLau, WKWen_HK
dc.contributor.authorMak, JCWen_HK
dc.contributor.authorChan, KHen_HK
dc.contributor.authorLaw, ACKen_HK
dc.date.accessioned2012-05-28T08:17:43Z-
dc.date.available2012-05-28T08:17:43Z-
dc.date.issued2012en_HK
dc.identifier.citationNeurotoxicity Research, 2012, v. 22 n. 2, p. 170-176en_HK
dc.identifier.issn1029-8428en_HK
dc.identifier.urihttp://hdl.handle.net/10722/147110-
dc.description.abstractThe author group has previously established an in vivo subchronic cigarette smoke (CS) exposure rat model, in which the systemic oxidative burden as well as the modulation of local anti-oxidative enzymes in the lung has been demonstrated. Oxidative stress has been shown to induce pro-inflammatory cytokine release, including interleukin (IL)-6 in the airways. In this study, we aimed to investigate the changes in IL-6 production, as well as the oxidative/anti-oxidative responses in the cerebral cortex using the same in vivo model. IL-6 was determined by RT-PCR and western-blot analysis. Local oxidative and anti-oxidative responses were determined by measuring cerebral cortical malondialdehyde (MDA) and advanced oxidation protein product (AOPP) levels, superoxide dismutase (SOD) and catalase activities, and the reduced to oxidized glutathione (GSH/GSSG) ratio. Nitrite level was measured by fluorescent spectrophotometry. Our results demonstrated a significant increase in both IL-6 mRNA and protein levels. Reductions of SOD activity and manganese (Mn)SOD protein level were observed together with the increased level of superoxide measured by chemiluminescent signal, after 56 days of CS exposure. There were no significant changes in the cerebral cortical levels of MDA, AOPP, catalase activity, and the GSH/GSSG ratio. Nitrite level was significantly reduced, together with the decreased protein level of nNOS in the cerebral cortex, after 56 days of CS exposure. Our results suggest that exposure to CS induces IL-6 expression in the cerebral cortex, which is not mediated by the oxidative/anti-oxidative imbalance. © 2012 Springer Science+Business Media, LLC.en_HK
dc.languageengen_US
dc.publisherF P Graham Publishing Company. The Journal's web site is located at http://www.fpgrahamco.com/Neuro/index.htmlen_HK
dc.relation.ispartofNeurotoxicity Researchen_HK
dc.rightsThe Author(s)en_US
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.en_US
dc.subjectNeuroinflammationen_HK
dc.subjectNitric oxideen_HK
dc.subjectReactive oxygen speciesen_HK
dc.subjectSmokingen_HK
dc.titleCigarette smoke-induced cerebral cortical interleukin-6 elevation is not mediated through oxidative stressen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://www.springerlink.com/link-out/?id=2104&code=2N37812223188545&MUD=MPen_US
dc.identifier.emailMak, JCW: judymak@hku.hken_HK
dc.identifier.emailLaw, ACK: acklaw@hku.hken_HK
dc.identifier.authorityMak, JCW=rp00352en_HK
dc.identifier.authorityLaw, ACK=rp00262en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1007/s12640-011-9301-8en_HK
dc.identifier.pmid22194160-
dc.identifier.scopuseid_2-s2.0-84865360580en_HK
dc.identifier.hkuros204392-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84865360580&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume22en_HK
dc.identifier.issue2en_HK
dc.identifier.spage170en_HK
dc.identifier.epage176en_HK
dc.identifier.eissn1476-3524en_US
dc.identifier.isiWOS:000305010100008-
dc.publisher.placeUnited Statesen_HK
dc.description.otherSpringer Open Choice, 28 May 2012en_US
dc.identifier.scopusauthoridLau, WKW=35292424400en_HK
dc.identifier.scopusauthoridMak, JCW=7103323094en_HK
dc.identifier.scopusauthoridChan, KH=23396210000en_HK
dc.identifier.scopusauthoridLaw, ACK=26323772800en_HK
dc.identifier.issnl1029-8428-

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