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Conference Paper: Protection of cigarette smoke–induced up-regulation of neutrophil elastase by Chinese green tea in rat lung

TitleProtection of cigarette smoke–induced up-regulation of neutrophil elastase by Chinese green tea in rat lung
Authors
Issue Date2009
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/
Citation
The 14th Medical Research Conference, Department of Medicine, The University of Hong Kong, Hong Kong, 10 January 2009. In Hong Kong Medical Journal, 2009, v. 15 n. Supp 1, p. 8 How to Cite?
AbstractIntroduction: Chronic obstructive pulmonary disease (COPD) is a progressively destructive airway disease mainly caused by smoking. Protease/anti-protease imbalance is hypothesised in the pathogenesis of COPD. Many studies have shown that the activities of proteases overwhelmed anti-proteases, causing lung destruction. Neutrophil elastase (NE) is one such protease released by neutrophil degranulation. This study aimed to investigate whether cigarette smoke (CS) exposure would up-regulate NE in bronchial secretions and whether Chinese green tea consumption would control the NE level/activity in the secretions. Methods: Sprague-Dawley rats were divided into four groups, ie sham air, 4% CS, 2% Lung Chen tea plus sham air or 4% CS. Exposure to sham air or 4% CS was performed for 1 hour/day for 56 days in ventilated smoking chambers. Rat lung tissues and bronchoalveolar lavage fluid (BALF) were obtained from rats sacrificed 24 hours after last CS exposure. Activity and amount of NE were determined by activity assay and ELISA analysis respectively. Results: NE activity was higher in BALF than in lung homogenates. There was a significant increase for NE activity in both lung homogenates (29.37±6.26 nM and 1.29±1.22 nM for CS-exposed and sham-air rats respectively; P<0.001) and BALF (43.47±3.15 nM and undetectable level for CS-exposed and sham-air rats respectively; P<0.001). The total amount of NE protein was also increased in BALF after CS exposure. The elevated CS-induced NE activity was prevented by green tea consumption (6.34±5.00 nM and 26.33±1.39 nM for lung homogenates and BALF respectively; P<0.001). Conclusion: These preliminary data suggest that Chinese green tea might have the ability to suppress CS-induced upregulation of NE activity and protein in lung. Further studies will be needed to elucidate the mechanism by which green tea regulates bronchial NE level in lung injury. Acknowledgement: This research was supported by Hong Kong Lung Foundation Research Grant.
Persistent Identifierhttp://hdl.handle.net/10722/61546
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorChan, KH-
dc.contributor.authorChan, CH-
dc.contributor.authorHo, SP-
dc.contributor.authorYeung, SC-
dc.contributor.authorShum, DKY-
dc.contributor.authorIp, MSM-
dc.contributor.authorMan, RYK-
dc.contributor.authorMak, JCW-
dc.date.accessioned2010-07-13T03:42:08Z-
dc.date.available2010-07-13T03:42:08Z-
dc.date.issued2009-
dc.identifier.citationThe 14th Medical Research Conference, Department of Medicine, The University of Hong Kong, Hong Kong, 10 January 2009. In Hong Kong Medical Journal, 2009, v. 15 n. Supp 1, p. 8-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/61546-
dc.description.abstractIntroduction: Chronic obstructive pulmonary disease (COPD) is a progressively destructive airway disease mainly caused by smoking. Protease/anti-protease imbalance is hypothesised in the pathogenesis of COPD. Many studies have shown that the activities of proteases overwhelmed anti-proteases, causing lung destruction. Neutrophil elastase (NE) is one such protease released by neutrophil degranulation. This study aimed to investigate whether cigarette smoke (CS) exposure would up-regulate NE in bronchial secretions and whether Chinese green tea consumption would control the NE level/activity in the secretions. Methods: Sprague-Dawley rats were divided into four groups, ie sham air, 4% CS, 2% Lung Chen tea plus sham air or 4% CS. Exposure to sham air or 4% CS was performed for 1 hour/day for 56 days in ventilated smoking chambers. Rat lung tissues and bronchoalveolar lavage fluid (BALF) were obtained from rats sacrificed 24 hours after last CS exposure. Activity and amount of NE were determined by activity assay and ELISA analysis respectively. Results: NE activity was higher in BALF than in lung homogenates. There was a significant increase for NE activity in both lung homogenates (29.37±6.26 nM and 1.29±1.22 nM for CS-exposed and sham-air rats respectively; P<0.001) and BALF (43.47±3.15 nM and undetectable level for CS-exposed and sham-air rats respectively; P<0.001). The total amount of NE protein was also increased in BALF after CS exposure. The elevated CS-induced NE activity was prevented by green tea consumption (6.34±5.00 nM and 26.33±1.39 nM for lung homogenates and BALF respectively; P<0.001). Conclusion: These preliminary data suggest that Chinese green tea might have the ability to suppress CS-induced upregulation of NE activity and protein in lung. Further studies will be needed to elucidate the mechanism by which green tea regulates bronchial NE level in lung injury. Acknowledgement: This research was supported by Hong Kong Lung Foundation Research Grant.-
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.titleProtection of cigarette smoke–induced up-regulation of neutrophil elastase by Chinese green tea in rat lung-
dc.typeConference_Paper-
dc.identifier.emailChan, CH: bcsty99@HKUCC.hku.hk-
dc.identifier.emailYeung, SC: yeungsc@HKUCC.hku.hk-
dc.identifier.emailShum, DKY: shumdkhk@hkucc.hku.hk-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hk-
dc.identifier.emailMak, JCW: judymak@HKUCC.hku.hk-
dc.identifier.authorityShum, DKY=rp00321-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.authorityMan, RYK=rp00236-
dc.identifier.authorityMak, JCW=rp00352-
dc.identifier.hkuros162747-
dc.identifier.volume15-
dc.identifier.issueSupp 1-
dc.identifier.spage8-
dc.identifier.epage8-
dc.publisher.placeHong Kong-

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