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- Publisher Website: 10.1016/j.phymed.2018.11.028
- Scopus: eid_2-s2.0-85064323432
- PMID: 31005721
- WOS: WOS:000473047100010
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Article: (-)-Epigallocatechin-3-gallate suppresses cigarette smoke-induced inflammation in human cardiomyocytes via ROS-mediated MAPK and NF-κB pathways
Title | (-)-Epigallocatechin-3-gallate suppresses cigarette smoke-induced inflammation in human cardiomyocytes via ROS-mediated MAPK and NF-κB pathways |
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Authors | |
Keywords | acetylcysteine antioxidant cigarette smoke epigallocatechin gallate immunoglobulin enhancer binding protein |
Issue Date | 2019 |
Publisher | Elsevier GmbH - Urban und Fischer Verlag. The Journal's web site is located at http://www.elsevier.com/locate/phytomed |
Citation | Phytomedicine, 2019, v. 58, p. article no. 152768 How to Cite? |
Abstract | BACKGROUND
Cigarette smoking is the leading cause for the initiation and development of cardiovascular disease (CVD). Oxidative stress and inflammatory responses play important roles in the pathophysiological processes of smoking-induced cardiac injury. (-)-epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea, which is made from Camellia sinensis leaves, has been reported to possess potent anti-oxidant property.
PURPOSE
This study aims to investigate whether the antioxidant EGCG could alleviate cigarette smoke medium (CSM)-induced inflammation in human AC16 cardiomyocytes in vitro.
METHODS
Human AC16 cardiomyocytes were pre-treated with EGCG, N-acetyl-L-cysteine (NAC), or specific inhibitors for 30 min before 4% CSM was added. Supernatant was collected for determination of interleukin (IL)-8 by ELISA and cells were collected for flow cytometry, biochemical assays and Western blot analysis.
RESULTS
EGCG treatment significantly attenuated CSM-induced oxidative stress as evidenced by reducing intracellular and mitochondrial reactive oxygen species (ROS) generations and preventing antioxidant depletion. EGCG treatment reduced CSM-induced inflammatory chemokine interleukin (IL)-8 productions in the supernatant via the inhibition of ERK1/2, p38 MAPK and NF-κB pathways. EGCG treatment further inhibited CSM-induced cell apoptosis.
CONCLUSION
Taken together, EGCG protected against CSM-induced inflammation and cell apoptosis by attenuating oxidative stress via inhibiting ERK1/2, p38 MAPK, and NF-κB activation in AC16 cardiomyocytes. These findings suggest that EGCG with its antioxidant, anti-inflammatory and anti-apoptotic properties may act as a promising cardioprotective agent against ROS-mediated cardiac injury. |
Persistent Identifier | http://hdl.handle.net/10722/273400 |
ISSN | 2023 Impact Factor: 6.7 2023 SCImago Journal Rankings: 1.267 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Liang, Y | - |
dc.contributor.author | Ip, MSM | - |
dc.contributor.author | Mak, JCW | - |
dc.date.accessioned | 2019-08-06T09:28:15Z | - |
dc.date.available | 2019-08-06T09:28:15Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Phytomedicine, 2019, v. 58, p. article no. 152768 | - |
dc.identifier.issn | 0944-7113 | - |
dc.identifier.uri | http://hdl.handle.net/10722/273400 | - |
dc.description.abstract | BACKGROUND Cigarette smoking is the leading cause for the initiation and development of cardiovascular disease (CVD). Oxidative stress and inflammatory responses play important roles in the pathophysiological processes of smoking-induced cardiac injury. (-)-epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea, which is made from Camellia sinensis leaves, has been reported to possess potent anti-oxidant property. PURPOSE This study aims to investigate whether the antioxidant EGCG could alleviate cigarette smoke medium (CSM)-induced inflammation in human AC16 cardiomyocytes in vitro. METHODS Human AC16 cardiomyocytes were pre-treated with EGCG, N-acetyl-L-cysteine (NAC), or specific inhibitors for 30 min before 4% CSM was added. Supernatant was collected for determination of interleukin (IL)-8 by ELISA and cells were collected for flow cytometry, biochemical assays and Western blot analysis. RESULTS EGCG treatment significantly attenuated CSM-induced oxidative stress as evidenced by reducing intracellular and mitochondrial reactive oxygen species (ROS) generations and preventing antioxidant depletion. EGCG treatment reduced CSM-induced inflammatory chemokine interleukin (IL)-8 productions in the supernatant via the inhibition of ERK1/2, p38 MAPK and NF-κB pathways. EGCG treatment further inhibited CSM-induced cell apoptosis. CONCLUSION Taken together, EGCG protected against CSM-induced inflammation and cell apoptosis by attenuating oxidative stress via inhibiting ERK1/2, p38 MAPK, and NF-κB activation in AC16 cardiomyocytes. These findings suggest that EGCG with its antioxidant, anti-inflammatory and anti-apoptotic properties may act as a promising cardioprotective agent against ROS-mediated cardiac injury. | - |
dc.language | eng | - |
dc.publisher | Elsevier GmbH - Urban und Fischer Verlag. The Journal's web site is located at http://www.elsevier.com/locate/phytomed | - |
dc.relation.ispartof | Phytomedicine | - |
dc.subject | acetylcysteine | - |
dc.subject | antioxidant | - |
dc.subject | cigarette smoke | - |
dc.subject | epigallocatechin gallate | - |
dc.subject | immunoglobulin enhancer binding protein | - |
dc.title | (-)-Epigallocatechin-3-gallate suppresses cigarette smoke-induced inflammation in human cardiomyocytes via ROS-mediated MAPK and NF-κB pathways | - |
dc.type | Article | - |
dc.identifier.email | Liang, Y: 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.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.phymed.2018.11.028 | - |
dc.identifier.pmid | 31005721 | - |
dc.identifier.scopus | eid_2-s2.0-85064323432 | - |
dc.identifier.hkuros | 300322 | - |
dc.identifier.volume | 58 | - |
dc.identifier.spage | article no. 152768 | - |
dc.identifier.epage | article no. 152768 | - |
dc.identifier.isi | WOS:000473047100010 | - |
dc.publisher.place | Germany | - |
dc.identifier.issnl | 0944-7113 | - |