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

TitleEffects of epigallocatechin gallate on cigarette smoke-induced oxidative stress and apoptosis in rat lung in vivo
Authors
Issue Date2015
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/
Citation
The 20th Medical Research Conference (MRC 2015), The University of Hong Kong, Hong Kong, 17 January 2015. In Hong Kong Medical Journal, 2015, v. 21 n. 1 suppl., p. 19, abstract no. 20 How to Cite?
AbstractBACKGROUND: Cigarette smoking is the major risk factor for the development of chronic obstructive pulmonary disease. 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, has long been considered as an antioxidant. The aim of this study was 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 equally and randomly divided into four treatment 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 throughout the experimental period. 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 apoptosis-related protein caspase-3 (total and cleaved) and Bcl-2 were detected by Western blot analysis. RESULTS: CS exposure alone caused an increase in protein expression of NQO1, Bcl-2, and cleaved caspase-3 in comparison to control group. On the other hand, EGCG alone also increased NQO1 but has no effect on Bcl-2 or caspase-3 (total and cleaved). The combination of EGCG and CS normalised 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. ACKNOWLEDGEMENT: This work was supported by the Hong Kong Research Grant Council General Research Fund (RGC_GRF) 2012-2013 (HKU 773612M).
Persistent Identifierhttp://hdl.handle.net/10722/232405
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorCui, Y-
dc.contributor.authorLiang, YM-
dc.contributor.authorIp, MSM-
dc.contributor.authorMak, JCW-
dc.date.accessioned2016-09-20T05:29:46Z-
dc.date.available2016-09-20T05:29:46Z-
dc.date.issued2015-
dc.identifier.citationThe 20th Medical Research Conference (MRC 2015), The University of Hong Kong, Hong Kong, 17 January 2015. In Hong Kong Medical Journal, 2015, v. 21 n. 1 suppl., p. 19, abstract no. 20-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/232405-
dc.description.abstractBACKGROUND: Cigarette smoking is the major risk factor for the development of chronic obstructive pulmonary disease. 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, has long been considered as an antioxidant. The aim of this study was 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 equally and randomly divided into four treatment 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 throughout the experimental period. 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 apoptosis-related protein caspase-3 (total and cleaved) and Bcl-2 were detected by Western blot analysis. RESULTS: CS exposure alone caused an increase in protein expression of NQO1, Bcl-2, and cleaved caspase-3 in comparison to control group. On the other hand, EGCG alone also increased NQO1 but has no effect on Bcl-2 or caspase-3 (total and cleaved). The combination of EGCG and CS normalised 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. ACKNOWLEDGEMENT: This work was supported by the Hong Kong Research Grant Council General Research Fund (RGC_GRF) 2012-2013 (HKU 773612M). -
dc.languageeng-
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/-
dc.relation.ispartofHong Kong Medical Journal-
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.titleEffects of epigallocatechin gallate on cigarette smoke-induced oxidative stress and apoptosis in rat lung in vivo-
dc.typeConference_Paper-
dc.identifier.emailLiang, YM: winniell@hku.hk-
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.identifier.hkuros264113-
dc.identifier.volume21-
dc.identifier.issue1 suppl.-
dc.identifier.spage19, abstract no. 20-
dc.identifier.epage19, abstract no. 20-
dc.publisher.placeHong Kong-

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