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Article: Effects of the natural flavone trimethylapigenin on cardiac potassium currents
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TitleEffects of the natural flavone trimethylapigenin on cardiac potassium currents
 
AuthorsLiu, Y2 3
Xu, XH3
Liu, Z4
Du, XL4
Chen, KH2 3
Xin, X2 3
Jin, ZD3
Shen, JZ2 3
Hu, Y2 3
Li, GR1
Jin, MW2 3
 
KeywordsAcetylcholine-Activated K + Current
Hkv1.5
Open Channel Blocker
Trimethylapigenin
 
Issue Date2012
 
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm
 
CitationBiochemical Pharmacology, 2012, v. 84 n. 4, p. 498-506 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bcp.2012.05.002
 
AbstractThe natural flavones and polymethylflavone have been reported to have cardiovascular protective effects. In the present study, we determined whether quecertin, apigenin and their methylated compounds (3,7,3′,4′-tetramethylquecertin, 3,5,7,3′,4′-pentamethylquecertin, 7,4′-dimethylapigenin, and 5,7,4′-trimethylapigenin) would block the atrial specific potassium channel hKv1.5 using a whole-cell patch voltage-clamp technique. We found that only trimethylapigenin showed a strong inhibitory effect on hKv1.5 channel current. This compound suppressed hKv1.5 current in HEK 293 cell line (IC 50 = 6.4 μM), and the ultra-rapid delayed rectify K + current I Kur in human atrial myocytes (IC 50 = 8.0 μM) by binding to the open channels and showed a use- and frequency-dependent manner. In addition, trimethylapigenin decreased transient outward potassium current (I to) in human atrial myocytes, inhibited acetylcholine-activated K + current (IC 50 = 6.8 μM) in rat atrial myocytes. Interestingly, trimethylapigenin had a weak inhibition of hERG channel current. Our results indicate that trimethyapigenin significantly inhibits the atrial potassium currents hKv1.5/I Kur and I KACh, which suggests that trimethylapigenin may be a potential candidate for anti-atrial fibrillation. © 2012 Elsevier Inc. All rights reserved.
 
ISSN0006-2952
2013 Impact Factor: 4.650
2013 SCImago Journal Rankings: 1.994
 
DOIhttp://dx.doi.org/10.1016/j.bcp.2012.05.002
 
ISI Accession Number IDWOS:000307135600011
 
DC FieldValue
dc.contributor.authorLiu, Y
 
dc.contributor.authorXu, XH
 
dc.contributor.authorLiu, Z
 
dc.contributor.authorDu, XL
 
dc.contributor.authorChen, KH
 
dc.contributor.authorXin, X
 
dc.contributor.authorJin, ZD
 
dc.contributor.authorShen, JZ
 
dc.contributor.authorHu, Y
 
dc.contributor.authorLi, GR
 
dc.contributor.authorJin, MW
 
dc.date.accessioned2012-09-05T05:32:16Z
 
dc.date.available2012-09-05T05:32:16Z
 
dc.date.issued2012
 
dc.description.abstractThe natural flavones and polymethylflavone have been reported to have cardiovascular protective effects. In the present study, we determined whether quecertin, apigenin and their methylated compounds (3,7,3′,4′-tetramethylquecertin, 3,5,7,3′,4′-pentamethylquecertin, 7,4′-dimethylapigenin, and 5,7,4′-trimethylapigenin) would block the atrial specific potassium channel hKv1.5 using a whole-cell patch voltage-clamp technique. We found that only trimethylapigenin showed a strong inhibitory effect on hKv1.5 channel current. This compound suppressed hKv1.5 current in HEK 293 cell line (IC 50 = 6.4 μM), and the ultra-rapid delayed rectify K + current I Kur in human atrial myocytes (IC 50 = 8.0 μM) by binding to the open channels and showed a use- and frequency-dependent manner. In addition, trimethylapigenin decreased transient outward potassium current (I to) in human atrial myocytes, inhibited acetylcholine-activated K + current (IC 50 = 6.8 μM) in rat atrial myocytes. Interestingly, trimethylapigenin had a weak inhibition of hERG channel current. Our results indicate that trimethyapigenin significantly inhibits the atrial potassium currents hKv1.5/I Kur and I KACh, which suggests that trimethylapigenin may be a potential candidate for anti-atrial fibrillation. © 2012 Elsevier Inc. All rights reserved.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationBiochemical Pharmacology, 2012, v. 84 n. 4, p. 498-506 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bcp.2012.05.002
 
dc.identifier.citeulike11092493
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.bcp.2012.05.002
 
dc.identifier.hkuros202912
 
dc.identifier.isiWOS:000307135600011
 
dc.identifier.issn0006-2952
2013 Impact Factor: 4.650
2013 SCImago Journal Rankings: 1.994
 
dc.identifier.pmid22583923
 
dc.identifier.scopuseid_2-s2.0-84864138148
 
dc.identifier.urihttp://hdl.handle.net/10722/163493
 
dc.languageeng
 
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm
 
dc.publisher.placeUnited States
 
dc.relation.ispartofBiochemical Pharmacology
 
dc.subjectAcetylcholine-Activated K + Current
 
dc.subjectHkv1.5
 
dc.subjectOpen Channel Blocker
 
dc.subjectTrimethylapigenin
 
dc.titleEffects of the natural flavone trimethylapigenin on cardiac potassium currents
 
dc.typeArticle
 
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<contributor.author>Xu, XH</contributor.author>
<contributor.author>Liu, Z</contributor.author>
<contributor.author>Du, XL</contributor.author>
<contributor.author>Chen, KH</contributor.author>
<contributor.author>Xin, X</contributor.author>
<contributor.author>Jin, ZD</contributor.author>
<contributor.author>Shen, JZ</contributor.author>
<contributor.author>Hu, Y</contributor.author>
<contributor.author>Li, GR</contributor.author>
<contributor.author>Jin, MW</contributor.author>
<date.accessioned>2012-09-05T05:32:16Z</date.accessioned>
<date.available>2012-09-05T05:32:16Z</date.available>
<date.issued>2012</date.issued>
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<description.abstract>The natural flavones and polymethylflavone have been reported to have cardiovascular protective effects. In the present study, we determined whether quecertin, apigenin and their methylated compounds (3,7,3&#8242;,4&#8242;-tetramethylquecertin, 3,5,7,3&#8242;,4&#8242;-pentamethylquecertin, 7,4&#8242;-dimethylapigenin, and 5,7,4&#8242;-trimethylapigenin) would block the atrial specific potassium channel hKv1.5 using a whole-cell patch voltage-clamp technique. We found that only trimethylapigenin showed a strong inhibitory effect on hKv1.5 channel current. This compound suppressed hKv1.5 current in HEK 293 cell line (IC 50 = 6.4 &#956;M), and the ultra-rapid delayed rectify K + current I Kur in human atrial myocytes (IC 50 = 8.0 &#956;M) by binding to the open channels and showed a use- and frequency-dependent manner. In addition, trimethylapigenin decreased transient outward potassium current (I to) in human atrial myocytes, inhibited acetylcholine-activated K + current (IC 50 = 6.8 &#956;M) in rat atrial myocytes. Interestingly, trimethylapigenin had a weak inhibition of hERG channel current. Our results indicate that trimethyapigenin significantly inhibits the atrial potassium currents hKv1.5/I Kur and I KACh, which suggests that trimethylapigenin may be a potential candidate for anti-atrial fibrillation. &#169; 2012 Elsevier Inc. All rights reserved.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province
  3. Tongji Medical College
  4. Huazhong University of Science and Technology