Journal of Oral Science Research ›› 2020, Vol. 36 ›› Issue (4): 377-381.DOI: 10.13701/j.cnki.kqyxyj.2020.04.017

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Effect of N-acetylcysteine on Inflammatory Injury Induced by Lipopolysaccharide in Vascular Endothelial Cells

ZHANG Zhenzhen, XIONG Ting, ZHENG Rui, HUANG Jialin, GUO Ling*   

  1. Department of Prosthodontics, Hospital of Stomatology,Southwest Medical University,Luzhou 646000,China
  • Received:2019-07-01 Online:2020-05-28 Published:2020-05-28

Abstract: Objective: To investigate whether N-acetylcysteine (NAC) has protective effects on lipopolysaccharide (LPS)-stimulated vascular endothelial cells, and provide a theoretical basis for the treatment of peri-implantitis and periodontitis. Methods: The effects of different concentrations of LPS or NAC on proliferation of human umbilical vein endothelial cells (HUVECs) were measured by cell counting kit 8 (CCK-8) to obtain the optimal drug concentration for stimulation of HUVECs. After adding the optimal drug concentration of LPS and/or NAC to treat HUVECs for 24 h, real-time semi-quantitative polymerase chain reaction (RT-qPCR) was used to detect the mRNA expression of inflammatory factors interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and cell adhesion molecule 1 (ICAM-1). Protein expression of TNF-α and IL-8 were detected by enzyme-linked immunosorbent assay (ELISA). The protein expressions of ICAM-1 and NF-κB signaling pathway were detected by western blot. Results: LPS stimulated HUVECs to overexpress inflammatory factors TNF-α, IL-8, and ICAM-1. In addition, LPS increased phosphorylation of P65 (pP65) expression in the NF-κB pathway. However, NAC pretreatment of HUVECs significantly inhibited the increase of TNF-α, IL-8, and ICAM-1 expression induced by LPS and decreased the secretion level of pP65. Conclusion: NAC protects HUVECs against LPS-mediated inflammatory reaction and alleviates inflammation. The underlying mechanism is related to the NF-κB pathway.

Key words: vascular endothelial cells, N-acetylcysteine, lipopolysaccharide, inflammatory response, NF-κB signaling pathway