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Conference Paper: Epigallocatechin gallate alleviated cigarette smoke-induced cardiac inflammation

TitleEpigallocatechin gallate alleviated cigarette smoke-induced cardiac inflammation
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?
AbstractINTRODUCTION: Cigarette smoke (CS) is recognized as a major cause of cardiovascular disease (CVD), particularly in those with chronic obstructive pulmonary disease (COPD). Oxidative stress and inflammatory responses may play an important role in the pathophysiological processes of CS-induced cardiac injury. The aim of this study is to investigate whether the antioxidant epigallocatechin gallate (EGCG) could alleviate cardiac inflammation in a rat model of passive smoking in vivo and in human AC16 cardiomyocytes in vitro. METHODS: Male Sprague-Dawley rats (n = 32) were randomly divided into 4 groups. Rats were exposed to either sham air as a control or 4% CS for one hour daily for 56 days. Oral gavage of EGCG (50 mg/kg) was administrated to one of sham air groups and one of CS groups every other day. Serum and heart tissues were collected for examination. Human AC16 cardiomyocytes was pretreated with EGCG (10 μM) for 30 min before 2% cigarette smoke medium (CSM) was added and incubated for an additional 24 h to collect supernatant. RESULTS: EGCG significantly reduced advanced oxidation protein products (AOPP, a protein oxidation marker) and increased anti-oxidant capacity (T-AOC) in serum and heart homogenates. Systemic and cardiac pro-inflammatory cytokines, cytokine-induced neutrophil chemoattractant-1 (CINC-1, resemble to human IL-8) and monocyte chemoattractant protein-1 (MCP-1) was increased in CS-exposed rats compared to control group, and EGCG normalized their levels. EGCG also abolished CSM-induced elevation of IL-8 release in human AC16 cardiomyocytes. CONCLUSION: Our data demonstrated that EGCG treatment could alleviate CS-induced inflammatory changes in the CS-exposed rat model and CSM-treated AC16 cell model, suggesting EGCG as a promising cardioprotective agent against cigarette smoke-mediated cardiac injury.
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/10722/213595
ISSN
2015 Impact Factor: 3.078
2015 SCImago Journal Rankings: 1.157

 

DC FieldValueLanguage
dc.contributor.authorLiang, Y-
dc.contributor.authorIp, MSM-
dc.contributor.authorMak, JCW-
dc.date.accessioned2015-08-06T07:22:25Z-
dc.date.available2015-08-06T07:22:25Z-
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/10722/213595-
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.abstractINTRODUCTION: Cigarette smoke (CS) is recognized as a major cause of cardiovascular disease (CVD), particularly in those with chronic obstructive pulmonary disease (COPD). Oxidative stress and inflammatory responses may play an important role in the pathophysiological processes of CS-induced cardiac injury. The aim of this study is to investigate whether the antioxidant epigallocatechin gallate (EGCG) could alleviate cardiac inflammation in a rat model of passive smoking in vivo and in human AC16 cardiomyocytes in vitro. METHODS: Male Sprague-Dawley rats (n = 32) were randomly divided into 4 groups. Rats were exposed to either sham air as a control or 4% CS for one hour daily for 56 days. Oral gavage of EGCG (50 mg/kg) was administrated to one of sham air groups and one of CS groups every other day. Serum and heart tissues were collected for examination. Human AC16 cardiomyocytes was pretreated with EGCG (10 μM) for 30 min before 2% cigarette smoke medium (CSM) was added and incubated for an additional 24 h to collect supernatant. RESULTS: EGCG significantly reduced advanced oxidation protein products (AOPP, a protein oxidation marker) and increased anti-oxidant capacity (T-AOC) in serum and heart homogenates. Systemic and cardiac pro-inflammatory cytokines, cytokine-induced neutrophil chemoattractant-1 (CINC-1, resemble to human IL-8) and monocyte chemoattractant protein-1 (MCP-1) was increased in CS-exposed rats compared to control group, and EGCG normalized their levels. EGCG also abolished CSM-induced elevation of IL-8 release in human AC16 cardiomyocytes. CONCLUSION: Our data demonstrated that EGCG treatment could alleviate CS-induced inflammatory changes in the CS-exposed rat model and CSM-treated AC16 cell model, suggesting EGCG as a promising cardioprotective agent against cigarette smoke-mediated cardiac injury.-
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.rightsPreprint This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article]. Authors are not required to remove preprints posted prior to acceptance of the submitted version. Postprint This is the accepted version of the following article: [full citation], which has been published in final form at [Link to final article].-
dc.rightsAuthor holds the copyright-
dc.subjectMedical Sciences-
dc.titleEpigallocatechin gallate alleviated cigarette smoke-induced cardiac inflammation-
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.hkuros246127-
dc.identifier.volume20-
dc.identifier.issuesuppl. S1-
dc.identifier.spage11-
dc.identifier.epage11-
dc.publisher.placeAustralia-

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