Tea polyphenols promote cardiac function and energy metabolism in ex vivo rat heart with ischemic/reperfusion injury and inhibit calcium inward current in cultured rat cardiac myocytes.
- Author:
Hua-Jin DONG
1
;
Jie LI
;
Hao ZHAN
;
Yang LI
;
Rui-Bin SU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcium; metabolism; Calcium Channels; metabolism; Cells, Cultured; Energy Metabolism; Heart; drug effects; In Vitro Techniques; Myocardial Reperfusion Injury; Myocardium; metabolism; Myocytes, Cardiac; drug effects; metabolism; Polyphenols; pharmacology; Rats; Tea; chemistry
- From: Journal of Southern Medical University 2016;36(5):604-608
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the protective effects of tea polyphenols (TP) against myocardial ischemia/reperfusion (IR) injuries and explore the possible mechanisms.
METHODSLangendorff-perfused rat hearts were subjected to ischemia for 30 min followed by reperfusion for another 30 min. Myocardial function indices were measured by a left ventricular cannula via a pressure transducer connected to the polygraph in isolated Langendorff hearts and energy metabolism was measured using (31)P nuclear magnetic resonance (NMR) spectroscopy. Whole-cell atch-clamp technique was used to record calcium inward current (I(Ca-L)) in cultured rat cardiac myocytes.
RESULTSCompared with the control hearts, the ex vivo rat hearts with 2.5 mg/L TP treatment showed significantly increased left ventricular developed pressure (LVDP), maximal rise rate of LVDP (+dp/d(tmax)), maximal fall rate of LVDP (-dp/dt(max)), and coronary flow (CF) (P<0.05). During both cardiac ischemia and reperfusion phase, ATP and PCr levels were elevated significantly in TP-treated hearts compared with those in the control hearts (P<0.05). In cultured rat cardiac myocytes, ICa-L was remarkably decreased by TP at the doses of 2.5 and 5.0 mg/L (P<0.01).
CONCLUSIONOur results support a possible protective role of TP against myocardial IR injury by improving myocardial energy metabolism and inhibiting I(Ca-L) in the cardiac myocytes.
