Abstract: Objective To explore whether Zn+2 can be used in peritoneal dialysis, we investigated the effect of Zn + 2 on lipopolysaccharide (LPS)- induced cell apoptosis in rat peritoneal mesothelial cells (RPMCs) and its underlying mechanism. Methods RPMCs were isolated by enzyme disaggregation, cultured, and then identified by phase contrast microscopy, transmission electron microscopy, and immunocytochemistry methods. RPMCs were incubated with 100 μg/ml LPS for 24 hours, or stimulated by 100 μg/ml LPS after incubation with 50 μM ZnSO4 for 24 hours. RPMCs incubated in regular medium were used as the controls. The expressions of p-ERK, BAX, AIF, caspase 3, and caspase 9 were assayed by western blot. Reactive oxygen species was measured by a reactive oxygen species assay kit. Results ZnSO4 significantly inhibited the LPS- induced RPMC apoptosis by attenuating ROS production, inhibiting LPS- induced BAX, AIF,
and the activation of caspase 3 and caspase 9. Further studies revealed that ZnSO4 treatment facilitated cell survival through the activation of ERK signaling pathway. Conclusion These results indicate that Zn+2 inhibits LPS-induced apoptosis in RPMCs by attenuating ROS production and inhibiting BAX, AIF, and the activation of caspase 3 and caspase 9. The ERK signaling pathway may take part in these changes.

Key words: lipopolysaccharide, ZnSO4, apoptosis, rat peritoneal mesothelial cells, peritoneal dialysis