[Epigallocatechin-3-gallate Attenuates Myocardial Reperfusion Injury in Rats Through Activation of PI3K/Akt Signaling Pathway].

Objective: This study was designed to investigate whether epigallocatechin-3-gallate (EGCG) postconditioning protects the heart against ischemic-reperfusion injury (IRI), and to explore its potential mechanisms in a rat model.

Methods: Male Wistar rats were subjected to myocardial ischemia (30 min) and reperfusion (up to 2 h) and the rats were divided into sham group (SO) group, ischemia-reperfusion (I/R) model group and EGCG group. EGCG group were treated with EGCG (10 mg/kg) via intravenous infusion 5 min before reperfusion. Electrocardiogram were applied to record ventricular arrhythmia frequency. The severity of myocardial injury [serum level of lactate dehydrogenase (LDH) and creatine kinase (CK), hematoxylineosin (HE) staining] and ventricular arrhythmia, and the serum levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukins-6 (IL-6) and IL-8] were assessed with ELISA, electrocardiogram and Western blot respectively.

Results: EGCG given before reperfusion could effectively reduce the serum level of LDH and CK and the incidence of ventricular arrhythmia (P < 0.05, respectively), improved the pathological damage. Meanwhile, EGCG could down-regulate the expression levels of TNF-α, IL-6, IL-8 in the myocardial tissue after IRI (P < 0.05, repectively). The expression levels of p-p85 and p-Akt in the EGCG group were significantly up-regulated compared to those in I/R group (P < 0.05, repectively).

Conclusion: EGCG-related anti-inflammatory action could attenuate rat myocardial IRI and this cardioprotective effect might be activated through the PI3K/Akt pathway.