Journal of Oral Science Research ›› 2022, Vol. 38 ›› Issue (5): 436-441.DOI: 10.13701/j.cnki.kqyxyj.2022.05.010

Previous Articles     Next Articles

Study on COX-2 Expression and Signalling Pathway in HUVECs Induced by P.gingivalis Lipopolysaccharide

GAO Yuan, LI Jia, LI Weishan*   

  1. Department of Periodontal Mucosal Disease, Stomatological Hospital, Jiamusi University, Jiamusi 154000, China
  • Received:2021-12-27 Online:2022-05-28 Published:2022-05-20

Abstract: Objective: To study the effect of P.gingivalis lipopolysaccharide on Cyclooxygenase-2 (Cox-2) expression in human umbilical vein endothelial cells (HUVECs), and investigate whether p38MAPK and PI3K/Akt signalling pathways involved in the regulation of COX-2 expression in HUVECs by P.g-LPS. Methods: HUVECs were cultured in vitro, and different concentrations of P.g-LPS (0.5, 1.0, 5.0, and 10.0 μg/mL) were used for stimulation for 6, 18, 24, and 36 hours. The effect of P.g-LPS on cell proliferation of HUVECs was detected by CCK-8. The expressions of COX-2 protein and gene in HUVECs were detected by Western blot and RT-qPCR. Additional, after stimulated with different concentrations of P.g-LPS(0.5, 1.0, 5.0, and 10.0 μg/mL)for 36 hours, HUVECs were added with pathway inhibitors SB203580 and LY294002. The expressions of COX-2 protein and gene in each group were detected by Western blot and RT-qPCR. Results: The proliferation activity of HUVECs decreased significantly with increasing P.g-LPS concentration (P<0.05). Compared with the control group, P.g-LPS promoted the expression of COX-2 in HUVECs in a concentration dependent manner (P<0.05). In addition, P.g-LPS activated the p38MAPK and PI3K/Akt signalling pathways. Addition of SB203580 and LY294002 inhibitors inhibited the expression of COX-2 by P.g-LPS (P<0.05). Conclusion: P.g-LPS can significantly inhibit the proliferation of HUVECs and may promote COX-2 protein and genes expression through activation of p38MAPK and PI3K/Akt pathways.

Key words: P.gingivalis lipopolysaccharide, human umbilical vein endothelial cells, cyclooxygenase-2, periodontitis, atherosclerosis