Abstract:

 [Abstract] Objective To investigate that the effects of Zn on lipopolysaccharide (LPS)-induced epithelial-to-mesenchymal transition (EMT) in rat PMCs (RPMCs) and examined the underlying molecular mechanisms. Methodology: RPMCs were isolated, cultured and passaged by enzymatic disaggregation, then identified by phase contrast inverted microscope, transmission electron microscope with immunocytochemistry method. RPMCs were incubated with 100μM LPS for 48 hours, or pre-incubated with 30μM ZnSO4 for 24 hours with stimulated by 100μM LPS for 48 hours. RPMCs in the control group were just incubated with medium. The expressions of α-SMA, E-cadherin , collagen I were detected by RT-PCR and the expressions of  NF-κB, I-κB p-NF-κB, p-I-κB were determined by western blotting. In addition, reactive oxygen species (ROS) assay experiments were performed using the ROS assay kit. Results: Zn supplementation inhibited LPS-induced RPMC EMT significantly, by attenuating ROS assay production. Whereas this LPS-induced EMT could be attenuated by pre-treating the RPMCs with 30 μM ZnSO4, which were evidenced by the reduced up-regulation of α-SMA and collagen I and the ameliorated expression of epithelial protein E-cadherin. Further analysis revealed that Zn supplementation inhibited LPS-induced RPMC EMT likely through inhibition of NF-κB pathways.  Conclusion: These results indicate that Zn can inhibit EMT in LPS-induced RPMCs by inhibition of oxidative stress as well as NF-κB pathways activation.

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