Lipopolysaccharide-induced suppression of periodontal ligament cell proliferation and apoptosis are strengthened under high glucose conditions

- Primary cultures of human PDL cells were prepared from extracted teeth of patients.
- LPS-induced suppression of cell proliferation were strengthened by high glucose.
- LPS-induced cell apoptosis were strengthened under high glucose condition.
- LPS-induced decrease in Bcl-2/Bax ratio were strengthened by high glucose.
- Glucose and LPS had a significant interaction for cell apoptosis.

The present study aimed to investigate the effect of lipopolysaccharide (LPS) on the proliferation and apoptosis of human periodontal ligament (hPDL) cells under normal glucose or high glucose conditions. Primary cultures of hPDL cells were prepared from extracted premolars of patients. The cells were incubated with 0, 1, or 10 μg/mL LPS under normal glucose (5.5 mmol/L) or high glucose (25 mmol/L) conditions for 24 h or 48 h. Cell proliferation was detected using a CCK-8 assay, and cell apoptosis was measured by Hoechst 33258 staining and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double staining. BCL2 and BAX mRNA and protein levels were measured by real-time polymerase chain reaction and western blotting, respectively. LPS (10 μg/mL) induced significant inhibition of cell proliferation and cell apoptosis, and a significant decrease in the BCL2/BAX ratio in the cells cultured with 5.5 mmol/L glucose. These effects of LPS were increased significantly in cells treated with 25 mmol/L glucose. Analysis of variance of the factorial design revealed that high glucose and LPS had a significant interaction for cell apoptosis, but not for cell proliferation. High glucose augmented LPS-induced hPDL cell apoptosis and cell proliferation inhibition. LPS and high glucose might interact to induce cell apoptosis.