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Article: Chinese green tea ameliorates lung injury in cigarette smoke-exposed rats

TitleChinese green tea ameliorates lung injury in cigarette smoke-exposed rats
Authors
KeywordsAirspace enlargement
Catalase
Chinese green tea (Lung Chen)
Cigarette smoke
Goblet cell
Superoxide dismutase
Issue Date2009
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmed
Citation
Respiratory Medicine, 2009, v. 103 n. 11, p. 1746-1754 How to Cite?
AbstractBackground: Epigallocatechin-3-gallate (EGCG), which has been shown to have potent antioxidant effect, comprises 80% of catechins in Chinese green tea. This study was to investigate whether cigarette smoke (CS) exposure would induce lung morphological changes and oxidative stress in the CS-exposed rat model, and whether Chinese green tea (Lung Chen tea with EGCG as its main active ingredient) consumption would alter oxidative stress in sera and lung leading to protection of CS-induced lung damage. Methods: Sprague-Dawley rats were randomly divided into four groups, i.e. sham air (SA), 4% CS, 2% Lung Chen tea plus SA or 4% CS. Exposure to SA or 4% CS was performed for 1 h/day for 56 days in ventilated smoking chambers. Sera and lung tissues were collected 24 h after last CS exposure for histology and all biochemical assays. Results: Airspace enlargement and goblet cell hyperplasia were observed after 56-day CS exposure alone, which were abolished in the presence of green tea consumption. Serum 8-isoprostane level was significantly elevated (p < 0.01) as well as lung superoxide dismutase (SOD) and catalase activities in CS-exposed rats compared to SA-exposed rats (p < 0.05), which returned to the levels of SA-exposed rats after Chinese green tea consumption. Conclusion: These results indicate that increased levels of systemic oxidative stress after CS exposure play an important role in the induction of lung damage. Chinese green tea may have the ability to suppress CS-induced oxidative stress that leads to protection of lung injury. © 2009 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/123932
ISSN
2021 Impact Factor: 4.582
2020 SCImago Journal Rankings: 1.316
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Lung Foundation
Funding Information:

This work was supported by a grant from the Hong Kong Lung Foundation.

References

 

DC FieldValueLanguage
dc.contributor.authorChan, KHen_HK
dc.contributor.authorHo, SPen_HK
dc.contributor.authorYeung, SCen_HK
dc.contributor.authorSo, WHLen_HK
dc.contributor.authorCho, CHen_HK
dc.contributor.authorKoo, MWLen_HK
dc.contributor.authorLam, WKen_HK
dc.contributor.authorIp, MSMen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorMak, JCWen_HK
dc.date.accessioned2010-10-11T02:16:26Z-
dc.date.available2010-10-11T02:16:26Z-
dc.date.issued2009en_HK
dc.identifier.citationRespiratory Medicine, 2009, v. 103 n. 11, p. 1746-1754en_HK
dc.identifier.issn0954-6111en_HK
dc.identifier.urihttp://hdl.handle.net/10722/123932-
dc.description.abstractBackground: Epigallocatechin-3-gallate (EGCG), which has been shown to have potent antioxidant effect, comprises 80% of catechins in Chinese green tea. This study was to investigate whether cigarette smoke (CS) exposure would induce lung morphological changes and oxidative stress in the CS-exposed rat model, and whether Chinese green tea (Lung Chen tea with EGCG as its main active ingredient) consumption would alter oxidative stress in sera and lung leading to protection of CS-induced lung damage. Methods: Sprague-Dawley rats were randomly divided into four groups, i.e. sham air (SA), 4% CS, 2% Lung Chen tea plus SA or 4% CS. Exposure to SA or 4% CS was performed for 1 h/day for 56 days in ventilated smoking chambers. Sera and lung tissues were collected 24 h after last CS exposure for histology and all biochemical assays. Results: Airspace enlargement and goblet cell hyperplasia were observed after 56-day CS exposure alone, which were abolished in the presence of green tea consumption. Serum 8-isoprostane level was significantly elevated (p < 0.01) as well as lung superoxide dismutase (SOD) and catalase activities in CS-exposed rats compared to SA-exposed rats (p < 0.05), which returned to the levels of SA-exposed rats after Chinese green tea consumption. Conclusion: These results indicate that increased levels of systemic oxidative stress after CS exposure play an important role in the induction of lung damage. Chinese green tea may have the ability to suppress CS-induced oxidative stress that leads to protection of lung injury. © 2009 Elsevier Ltd. All rights reserved.en_HK
dc.languageeng-
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmeden_HK
dc.relation.ispartofRespiratory Medicineen_HK
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAirspace enlargementen_HK
dc.subjectCatalaseen_HK
dc.subjectChinese green tea (Lung Chen)en_HK
dc.subjectCigarette smokeen_HK
dc.subjectGoblet cellen_HK
dc.subjectSuperoxide dismutaseen_HK
dc.subject.meshAntioxidants - pharmacology-
dc.subject.meshCatechin - analogs and derivatives - pharmacology-
dc.subject.meshGoblet Cells - drug effects - pathology-
dc.subject.meshLung Injury - drug therapy-
dc.subject.meshOxidative Stress - drug effects-
dc.titleChinese green tea ameliorates lung injury in cigarette smoke-exposed ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0954-6111&volume=103&issue=11&spage=1746&epage=1754&date=2009&atitle=Chinese+green+tea+ameliorates+lung+injury+in+cigarette+smoke-exposed+rats-
dc.identifier.emailKoo, MWL: wlkoo@hku.hken_HK
dc.identifier.emailIp, MSM: msmip@hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailMak, JCW: judymak@hku.hken_HK
dc.identifier.authorityKoo, MWL=rp00233en_HK
dc.identifier.authorityIp, MSM=rp00347en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.authorityMak, JCW=rp00352en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1016/j.rmed.2009.04.027en_HK
dc.identifier.pmid19487113en_HK
dc.identifier.scopuseid_2-s2.0-70349628613en_HK
dc.identifier.hkuros171589-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70349628613&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume103en_HK
dc.identifier.issue11en_HK
dc.identifier.spage1746en_HK
dc.identifier.epage1754en_HK
dc.identifier.eissn1532-3064-
dc.identifier.isiWOS:000271156500021-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, KH=7406035589en_HK
dc.identifier.scopusauthoridHo, SP=12794365900en_HK
dc.identifier.scopusauthoridYeung, SC=25923636600en_HK
dc.identifier.scopusauthoridSo, WHL=7004974020en_HK
dc.identifier.scopusauthoridCho, CH=35228665500en_HK
dc.identifier.scopusauthoridKoo, MWL=7004550899en_HK
dc.identifier.scopusauthoridLam, WK=35934675100en_HK
dc.identifier.scopusauthoridIp, MSM=7102423259en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.scopusauthoridMak, JCW=7103323094en_HK
dc.identifier.issnl0954-6111-

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