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Conference Paper: Effects of epigallocatechin gallate on cigarette smoke-induced oxidative stress and apoptosis in rat lung in vivo
Title | Effects of epigallocatechin gallate on cigarette smoke-induced oxidative stress and apoptosis in rat lung in vivo |
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Authors | |
Issue Date | 2015 |
Publisher | Hong 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? |
Abstract | BACKGROUND: 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).
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Persistent Identifier | http://hdl.handle.net/10722/232405 |
ISSN | 2023 Impact Factor: 3.1 2023 SCImago Journal Rankings: 0.261 |
DC Field | Value | Language |
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dc.contributor.author | Cui, Y | - |
dc.contributor.author | Liang, YM | - |
dc.contributor.author | Ip, MSM | - |
dc.contributor.author | Mak, JCW | - |
dc.date.accessioned | 2016-09-20T05:29:46Z | - |
dc.date.available | 2016-09-20T05:29:46Z | - |
dc.date.issued | 2015 | - |
dc.identifier.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 | - |
dc.identifier.issn | 1024-2708 | - |
dc.identifier.uri | http://hdl.handle.net/10722/232405 | - |
dc.description.abstract | BACKGROUND: 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.language | eng | - |
dc.publisher | Hong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/ | - |
dc.relation.ispartof | Hong Kong Medical Journal | - |
dc.rights | Hong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press. | - |
dc.title | Effects of epigallocatechin gallate on cigarette smoke-induced oxidative stress and apoptosis in rat lung in vivo | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Liang, YM: winniell@hku.hk | - |
dc.identifier.email | Ip, MSM: msmip@hku.hk | - |
dc.identifier.email | Mak, JCW: judithmak@hku.hk | - |
dc.identifier.authority | Ip, MSM=rp00347 | - |
dc.identifier.authority | Mak, JCW=rp00352 | - |
dc.identifier.hkuros | 264113 | - |
dc.identifier.volume | 21 | - |
dc.identifier.issue | 1 suppl. | - |
dc.identifier.spage | 19, abstract no. 20 | - |
dc.identifier.epage | 19, abstract no. 20 | - |
dc.publisher.place | Hong Kong | - |
dc.identifier.issnl | 1024-2708 | - |