The protective effects of reparixin against endothelial ischemia-reperfusion injury

Myocardial ischemia is a lack of blood supply to myocardial tissue. Rapid reperfusion therapy is required to prevent myocardial infarction. However, ischemia and reperfusion contribute to myocardial and endothelial injury or ischemia-reperfusion injury (IRI). A pro-inflammatory cytokine interleukin-8 (IL-8/CXCL8) plays an important role in the activation of neutrophil accumulation and promotes endothelial dysfunction. Therefore, inhibition of IRI through the regulation of inflammation using a CXCL8 receptor inhibitor reparixin is an attractive target. The aim of this study is to evaluate the effect of reparixin on endothelial cell viability after IRI.

Human vascular endothelial cells (EA.hy926) were cultured and pretreated with reparixin at concentrations of 0-1 mg/ml. To simulate ischemia, the cells were exposed to simulated ischemia solution for 60 min. Then, the cells were given complete medium as reperfusion followed by treatment with reparixin and incubated for 24 h. Cell viability was tested using MTT assay.

Percentages of cell viability of reparixin-treated groups of 0.0625 mg/mL (67.88 ± 7.82% control) and 0.125 mg/mL (84.28 ± 4.68% control) were significantly higher than that of the IR group (44.31 ± 4.64% control) at P < 0.05. The percentage of cell viability in the 0.125 mg/mL reparixin-treated group was not significantly different compared to the control.

Pretreatment and treatment of endothelial cells with reparixin, which is a CXCL-8 receptor inhibitor, demonstrated a protective effect on cell viability after simulated ischemia-reperfusion. However, further studies to investigate the underlying mechanisms are needed.