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(−)‐Epigalocathine‐3‐gallate attenuates oxidative stress by modulation of redox signaling in H9c2 cultured rat cardiac myoblasts
Author(s) -
Liou YingMing,
Hsu GenSen
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1093.8
Subject(s) - oxidative stress , reactive oxygen species , viability assay , myocyte , intracellular , microbiology and biotechnology , cytosol , chemistry , oxidative phosphorylation , apoptosis , biochemistry , biology , enzyme
This study intended to explore the potential mechanism for the cardio‐protection of (−)‐epigalocathine‐3‐gallate (EGCg) on oxidative stress exerted by H 2 O 2 or ischemia/reperfusion (IR) injury in H9c2 cultured rat cardiac myoblasts. H9c2 is a myogenic cell line from embryonic rat heart ventricle. When oxidative stress was induced in H9c2 cells by 0.4 or 1 mM H 2 O 2 , pretreatment with EGCg from 10 to 25 μM effectively recovered cell viability. Similarly, 5, or 10, or 15 μM EGCg supplementations significantly increased viability of cardiac cells with IR‐simulated stress. The cardio‐protection of EGCg involved in oxidation stress appears to act by reducing reactive oxygen species (ROS) and intracellular Ca 2+ . Measurements of dichlorofluorescein diacetate fluorescence for ROS generation showed that adding 5–50 μM EGCg to H 2 O 2 ‐treated H9c2 cells reduced their ROS generation back to the control levels. Intracellular Ca 2+ measurements by fura‐2 also indicated that 20 μM EGCg effectively reduced cytosolic Ca 2+ overload in H 2 O 2 ‐disturbed H9c2 cells. This result is consistent with our recent findings in the rat model of IR that pretreatment with green tea extract protects cardiomyocytes from IR injury by preventing cytosolic Ca 2+ overload and ROS generation (Liou et al., Pflügers Archiv‐EJP, 2010) . In addition, EGCg exerted the opposing effect of H 2 O 2 ‐induced oxidative stress in cultured H9c2 cells by modulation of β‐catenin signaling and Cx43 phosphorylation/dephosphorylation. Taken together, this study suggested that EGCg might regulate β‐catenin and Cx43 signaling and benefit cardio‐protection via redox signaling in H9c2 cardiac cells. Grant: NSC‐98‐2320‐B‐005‐001‐MY2.