Journal of Oral Science Research ›› 2020, Vol. 36 ›› Issue (1): 75-78.DOI: 10.13701/j.cnki.kqyxyj.2020.01.018

Previous Articles     Next Articles

Effect of Porphyromonas Gingivalis Lipopolysaccharide on Expression of Cav-1 in HUVECs

ZUO Yuan,LI Weishan*   

  1. Department of Periodontal Membrane,Stomatological Hospital Affiliated to Jiamusi University,Jiamusi 154007, China
  • Received:2019-04-10 Online:2020-01-28 Published:2020-01-16

Abstract: Objective: To study the effect of P. gingivalis lipopolysaccharide (P. g-LPS) on the expression of caveolin-1 (Cav-1) in human umbilical vein endothelial cells (HUVECs), and to explore the relationship between P. g-LPS and atherosclerosis (AS). Methods: HUVECs were cultured in vitro, and different concentrations of P.g-LPS (0.5, 1.0, 5.0, 10.0 mg/L) were selected to induce for 6, 18, 24 and 36 hours. The effects of P.g-LPS on the proliferation of HUVECs were detected by EdU method, the expression of Cav-1 in HUVECs was detected by ELISA, and the expression of Cav-1 was detected by RT-PCR. Results: After co-culture of P.g-LPS and HUVECs, the proliferation activity of HUVECs decreased compared with the control group. With the increase of P.g-LPS concentration, the proliferation activity of HUVECs decreased significantly (P<0.05). Compared with the control group, the expression of Cav-1 protein in HUVECs induced by P.g-LPS increased for 18 hours, sustained high expression for 24 and 36 hours, with the highest expression level at 36 hours (P<0.05); the expression of Cav-1 gene in HUVECs induced by P.g-LPS increased for 18 hours, and the expression of Cav-1 gene increased with the increase of concentration at 24 and 36 hours (P<0.001). Conclusion: P.g-LPS can significantly inhibit the proliferation activity of HUVECs and up-regulate the protein and molecular level of Cav-1 cells. It is suggested that P.g-LPS infection may cause endothelial cell disfunction, thereby accelerating the occurrence and development of AS

Key words: porphyromonas gingivalis, lipopolysaccharide, human umbilical vein endothelial cells, caveolin-1 atherolerosis