HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 294/1/H345    most recent 00785.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Li, D. Articles by Xie, Z. Search for Related Content PubMed PubMed Citation Articles by Li, D. Articles by Xie, Z.

Identification of a PKC-dependent regulation of myocardial contraction by epicatechin-3-gallate

¹Department of Physiology and Pharmacology, Health Science Campus, University of Toledo, Toledo, Ohio; and ²Key Laboratory of Tea Biochemistry and Biotechnology, Ministry of Agriculture and Ministry of Education, Anhui Agricultural University, Hefei, Anhui, People's Republic of China

Submitted 6 July 2007 ; accepted in final form 17 October 2007

In this study, the effects of tea catechins and tea theaflavins on myocardial contraction were examined in isolated rat hearts using a Langendorff-perfusion system. We found that both tea catechins and theaflavins had positive inotropic effects on the myocardium. Of the tested chemicals, epicatechin-3-gallate (ECG) and theaflavin-3,3'-digallate (TF₄) appear to be the most effective tea catechin and theaflavin, respectively. Further studies of ECG-induced positive inotropy revealed the following insights. First, unlike digitalis drugs, ECG had no effect on intracellular Ca²⁺ level in cultured adult cardiac myocytes. Second, it activated PKC, but not PKC, in the isolated hearts as well as in cultured cells. Neither a phospholipase C (PLC) inhibitor (U73122) nor the antioxidant N-acetyl cysteine (NAC) affected the ECG-induced activation of PKC. Third, inhibition of PKC by either chelerythrine chloride (CHE) or PKC translocation inhibitor peptide (TIP) caused a partial reduction of ECG-induced increases in myocardial contraction. Moreover, NAC was also effective in reducing the effects of ECG on myocardial contraction. Finally, pretreatment of the heart with both CHE and NAC completely abolished ECG-induced inotropic effects on the heart. Together, these findings indicate that ECG can regulate myocardial contractility via a novel PKC-dependent signaling pathway.

theaflavin-3,3'-digallate; positive inotropy; protein kinase C; reactive oxygen species