The Protective Effect of Epigallocatechin-3 Gallate on Ischemia/Reperfusion Injury in Isolated Rat Hearts: Anex vivoApproach

Abstract

The aim of this study was to evaluate the preventive role of epigallocatechin-3 gallate (EGCG, a derivative of green tea) in ischemia/reperfusion (I/R) injury of isolated rat hearts. It has been suggested that EGCG has beneficial health effects, including prevention of cancer and heart disease, and it is also a potent antioxidant. Rat hearts were subjected to 20 min of normoxia, 20 min of zero-flow ischemia and then 50 min of reperfusion. EGCG was perfused 10 min before ischemia and during the whole reperfusion period. EGCG significantly increased left ventricular developed pressure (LVDP) and increased maximum positive and negative dP/dt (＋ /-dP/dtmax). EGCG also significantly increased the coronary flow (CF) at baseline before ischemia and at the onset of the reperfusion period. Moreover, EGCG decreased left ventricular end diastolic pressure (LVEDP). This study showed that lipid peroxydation was inhibited and Mn-SOD and catalase expressions were increased in the presence of EGCG. In addition, EGCG increased levels of Bcl-2, Mn-superoxide dismutase (SOD), and catalase expression and decreased levels of Bax and increased the ratio of Bcl-2/Bax in isolated rat hearts. Cleaved caspase-3 was decreased after EGCG treatment. EGCG markedly decreased the infarct size while attenuating the increase in lactate dehydrogenase (LDH) levels in the effluent. In summary, we suggest that EGCG has a protective effect on I/R-associated hemodynamic alteration and injury by acting as an antioxidant and anti-apoptotic agent in one.

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“…Apolipoprotein E-deficient mice given tea extract containing EGCG (0.8g/L) experienced 27% plaque coverage of the aorta compared to 36% in the control group, as well as 27% and 50% reductions in cholesterol and triglyceride levels, respectively (Miura et al, 2001). Piao and colleagues used rat hearts to show that treatment with EGCG before ischemia and during the entire reperfusion period resulted in decreased caspase 3 activity and a recovery of superoxide dismutase and catalase activity, which results in decreased cell death and oxidative damage, respectively (Piao et al, 2011). The study also found an increase in anti-apoptotic protein Bcl-2 expression and a decrease in pro-apoptotic protein Bax expression after treatment with EGCG.…”

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“…Además de restablecer la actividad de la proteína kinasa PKC, EGCG inhibe la caspasa-3 y activa la vía PI3K/Akt e inhibe la expresión de genes proapoptóticos Bax y Bad e induce genes antiapoptóticos como Bcl-2, Bcl-W y Bcl-X (Piao, et al, 2011).…”

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“…As to the effect on apoptosis, the expressions of Bax (pro-apoptotic protein) and Bcl-2 (anti-apoptotic protein) protein levels were prominently decreased and increased by EGCG, respectively (20). Anti-apoptotic effect was supported by the finding that EGCG decreased the ratio of cleaved caspase-3, an important indicator of apoptotic cell death (20). On the basis of these results, it was concluded that EGCG protection against cardiac I/R injury occurred by the prevention of apoptosis via regulation of Bcl-2 and Bax expression and by anti-oxidant effects (20).…”

“…Similarly, EGCG significantly inhibited the lipid peroxidation ratio and increased the expression of Mnsuperoxide dismutase (SOD) and CAT compared to those in I/R injury group (20). As to the effect on apoptosis, the expressions of Bax (pro-apoptotic protein) and Bcl-2 (anti-apoptotic protein) protein levels were prominently decreased and increased by EGCG, respectively (20). Anti-apoptotic effect was supported by the finding that EGCG decreased the ratio of cleaved caspase-3, an important indicator of apoptotic cell death (20).…”

“…Abbreviations: Ischemia-reperfusion (I/R) measurements of lactate dehydrogenase and infarct size (20). Similarly, EGCG significantly inhibited the lipid peroxidation ratio and increased the expression of Mnsuperoxide dismutase (SOD) and CAT compared to those in I/R injury group (20).…”