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Conference Paper: Effects of epigallocatechin gallate on smoke-induced oxidative stress and apoptosis in rat lung in vivo

TitleEffects of epigallocatechin gallate on smoke-induced oxidative stress and apoptosis in rat lung in vivo
Authors
KeywordsMedical Sciences
Issue Date2015
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/RES
Citation
The Airway Vista 2015, Seoul, Korea, 21–22 March 2015. In Respirology, 2015, v. 20 suppl. S1, p. 11 How to Cite?
AbstractBACKGROUND: Cigarette smoking is the major risk factor for the development of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) is a rich source of oxidants, and is thought to disrupt the oxidant-antioxidant balance in the lung, thus inducing apoptosis. Epigallocatechin gallate (EGCG), a natural compound found mainly in green tea, is considered as an antioxidant. The aim of this study is to explore the role of EGCG on CS-induced oxidative stress and apoptosis in a rat model of passive smoking. METHODS: Thirty-two male Sprague Dawley rats were randomly divided into four groups: Control, CS alone, EGCG alone, and combination of CS and EGCG. The control group was exposed to sham air, while the CS group was exposed to 4% CS for 1 hour daily. The EGCG and EGCG + CS groups were given EGCG (50 mg/kg; oral gavage) every other day. Rats were sacrificed 56 days later and protein was extracted from lung tissue. Protein expressions of the antioxidant enzyme quinone oxidoreductase 1 (NQO1), and apoptosisrelated protein caspase-3 (total and cleaved) and Bcl-2 were detected by Western analysis. RESULTS: CS exposure alone caused an increase in protein expression of NQO1, Bcl-2 and cleaved-caspase-3 in comparison to control group. EGCG alone increased NQO1 but has no effect on Bcl-2 or caspase-3 (total and cleaved). The combination of EGCG and CS normalized the levels of NQO1 and Bcl-2 protein expression. CONCLUSION: Our data reinforce the defensive role of EGCG against oxidative stress and apoptosis. The protective role of EGCG in reversing apoptosis in the CS-exposed rat lungs is thought to be mediated through induction of antioxidant mechanisms.
DescriptionPoster abstracts
This free journal suppl. entitled: Special Issue: Abstracts of the Airway Vista 2015, 21–22 March 2015, Seoul, Korea
Persistent Identifierhttp://hdl.handle.net/10722/213594
ISSN
2015 Impact Factor: 3.078
2015 SCImago Journal Rankings: 1.157

 

DC FieldValueLanguage
dc.contributor.authorCui, Y-
dc.contributor.authorLiang, Y-
dc.contributor.authorIp, MSM-
dc.contributor.authorMak, JCW-
dc.date.accessioned2015-08-06T07:08:13Z-
dc.date.available2015-08-06T07:08:13Z-
dc.date.issued2015-
dc.identifier.citationThe Airway Vista 2015, Seoul, Korea, 21–22 March 2015. In Respirology, 2015, v. 20 suppl. S1, p. 11-
dc.identifier.issn1323-7799-
dc.identifier.urihttp://hdl.handle.net/10722/213594-
dc.descriptionPoster abstracts-
dc.descriptionThis free journal suppl. entitled: Special Issue: Abstracts of the Airway Vista 2015, 21–22 March 2015, Seoul, Korea-
dc.description.abstractBACKGROUND: Cigarette smoking is the major risk factor for the development of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) is a rich source of oxidants, and is thought to disrupt the oxidant-antioxidant balance in the lung, thus inducing apoptosis. Epigallocatechin gallate (EGCG), a natural compound found mainly in green tea, is considered as an antioxidant. The aim of this study is to explore the role of EGCG on CS-induced oxidative stress and apoptosis in a rat model of passive smoking. METHODS: Thirty-two male Sprague Dawley rats were randomly divided into four groups: Control, CS alone, EGCG alone, and combination of CS and EGCG. The control group was exposed to sham air, while the CS group was exposed to 4% CS for 1 hour daily. The EGCG and EGCG + CS groups were given EGCG (50 mg/kg; oral gavage) every other day. Rats were sacrificed 56 days later and protein was extracted from lung tissue. Protein expressions of the antioxidant enzyme quinone oxidoreductase 1 (NQO1), and apoptosisrelated protein caspase-3 (total and cleaved) and Bcl-2 were detected by Western analysis. RESULTS: CS exposure alone caused an increase in protein expression of NQO1, Bcl-2 and cleaved-caspase-3 in comparison to control group. EGCG alone increased NQO1 but has no effect on Bcl-2 or caspase-3 (total and cleaved). The combination of EGCG and CS normalized the levels of NQO1 and Bcl-2 protein expression. CONCLUSION: Our data reinforce the defensive role of EGCG against oxidative stress and apoptosis. The protective role of EGCG in reversing apoptosis in the CS-exposed rat lungs is thought to be mediated through induction of antioxidant mechanisms.-
dc.languageeng-
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/RES-
dc.relation.ispartofRespirology-
dc.rightsAuthor holds the copyright-
dc.subjectMedical Sciences-
dc.titleEffects of epigallocatechin gallate on smoke-induced oxidative stress and apoptosis in rat lung in vivo-
dc.typeConference_Paper-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.emailMak, JCW: judithmak@hku.hk-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.authorityMak, JCW=rp00352-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/resp.12479-
dc.identifier.hkuros246125-
dc.identifier.volume20-
dc.identifier.issuesuppl. S1-
dc.identifier.spage11-
dc.identifier.epage11-
dc.publisher.placeAustralia-

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