Anti-inflammatory effect of remifentanil in lipopolysaccharide–stimulated amniotic epithelial cells
10.17245/jdapm.2019.19.5.253
- Author:
Cheul Hong KIM
1
;
Seong Soon JEONG
;
Soon Ji PARK
;
Eun Ji CHOI
;
Yeon Ha KIM
;
Ji Hye AHN
Author Information
1. Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute, Yangsan, Korea. anji1030@naver.com
- Publication Type:Original Article
- Keywords:
Amnion;
Inflammation;
Preterm labor;
Remifentanil
- MeSH:
Abscess;
Amnion;
Anesthesia, General;
Blotting, Western;
Cell Survival;
Dinoprostone;
Epithelial Cells;
Facial Bones;
Female;
Humans;
Inflammation;
Interleukins;
Neck;
NF-kappa B;
Obstetric Labor, Premature;
Phosphorylation;
Pregnancy;
Pregnant Women;
Premature Birth;
Prostaglandin-Endoperoxide Synthases;
Tumor Necrosis Factor-alpha;
Uterine Contraction
- From:Journal of Dental Anesthesia and Pain Medicine
2019;19(5):253-260
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Sometimes general anesthesia is required for dental surgery in pregnant women. Facial bone fractures or neck abscess should be treated immediately. Dental surgery, however, creates a stressful situation that can cause inflammation. Inflammatory responses are a well-known major cause of preterm labor and preterm birth. Here we demonstrate the effects of remifentanil on the factors related to preterm labor and its mechanism of action on amniotic-derived epithelial cells (WISH cells). METHODS: WISH cells were exposed to lipopolysaccharide (LPS) for 24 h and co-treated with various concentrations of remifentanil. MTT assays were performed to measure cell viability. To explain the effects of remifentanil on the factors related to inflammation in WISH cells, activation of nuclear factor kappa B (NF-κB) and p38 and the expression of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, cyclooxygenase (COX)2, and prostaglandin E (PGE)2 were quantified using western blotting and RT-PCR, respectively. RESULTS: Remifentanil did not affect WISH cell viability. In western blot analysis, co-treatment with remifentanil resulted in decreased phosphorylation of NF-κB, and expression of COX2 and PGE2 in LPS-induced inflammation, but the results were statistically significant only at low concentrations. Reduction of IL-1β and TNF-α expression was also observed with RT-PCR. CONCLUSION: Co-treatment with remifentanil does not affect the viability of WISH cells, but reduces the expression of the factors related to inflammation, which can induce uterine contraction and preterm labor. These findings provide evidence that remifentanil may inhibit uterine contraction and preterm labor in clinical settings.
