[Injurious effect of zinc deficiency on cardiomyocytes].

The aim of the present study was to investigate the effect of zinc deficiency on cardiomyocyte survival and the underlying mechanisms. Simulated zinc deficiency model was developed in H9c2 cardiac cells with zinc chelator N, N, N', N'-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN). MTT assay was used to evaluate cell viability.

[Resveratrol attenuates oxidant-induced mitochondrial damage in embryonic rat cardiomyocytes via inactivating GSK-3β].

Objective: To investigate the underlying mechanism of the protective effects of resveratrol on oxidant-induced mitochondrial damage in embryonic rat cardiomyocytes.

Methods: H9c2 cells, a permanent cell line derived from embryonic rat cardiac tissue, and then randomly divided into control group [PBS, cells exposed to H2O2 (600 µmol/L) for 20 min to induce mitochondrial oxidant damage], resveratrol group (0.01, 0.

Cardioprotection against reperfusion injury: updated mechanisms and strategies.

Early restoration of blood flow to the ischemic myocardium not only saves myocardium but also induces reperfusion injury. While no specific therapy to reduce reperfusion injury has yet been established, recent laboratory studies have shown that G protein-coupled receptor (GPCR) agonists, insulin, and postconditioning can effectively prevent reperfusion injury in various experimental settings and animal species. The potential mechanisms underlying the cardioprotection initiated by these interventions may include activation of the reperfusion injury salvage kinase (RISK) pathway, inactivation of glycogen synthase kinase 3beta (GSK-3beta), and modulation of mitochondrial permeability transition pore (mPTP) opening.