Polo-like kinase 1 protects intestinal epithelial cells from apoptosis during sepsis via the nuclear factor-κB pathway

To verify the importance of activation of NF-κB in LPS-induced apoptosis, HT29 cells were pre-treated with various concentrations of pyrrolidine dithiocarbamic acid (PDTC) to suppress the activity of NF-κB and then were treated with 30 μg/mL LPS for 24 h. Then we found that pre-treatment with PDTC significantly increased the expression levels of pro-caspase-3 and IκB-α [Figure 1C], which illustrates that inhibition of NF-κB reduced LPS-induced apoptosis in HT29 cells. PLK1, as the most evolutionarily conserved member of the polo sub-family, is a cell cycle-related kinase required for proper M-phase progression and plays critical roles in diverse biochemical and cellular processes such as apoptosis and proliferation in humans. Inhibiting NF-κB partially rescues the apoptosis induced by sepsis in vitro, and NF-κB activation is regulated by PLK1. [...]the PLK1-NF-κB pathway might be critical in sepsis-induced intestinal barrier dysfunction.