Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells
10.17245/jdapm.2022.22.5.369
- Author:
Cheul-Hong KIM
1
;
Sang-Hoon LEE
;
Ji-Young YOON
;
Eun-Jung KIM
;
Jong Hoon JOO
;
Yeon Ha KIM
;
Eun-Ji CHOI
Author Information
1. Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute, Yangsan, Korea
- Publication Type:Original Article
- From:Journal of Dental Anesthesia and Pain Medicine
2022;22(5):369-376
- CountryRepublic of Korea
- Language:English
-
Abstract:
Background:Nonobstetric surgery is sometimes required during pregnancy, and neck abscess or facial bone fracture surgery cannot be postponed in pregnant women. However, dental surgery can be stressful and can cause inflammation, and the inflammatory response is a well-known major cause of preterm labor. Propofol is an intravenous anesthetic commonly used for general anesthesia and sedation. Studies investigating the effect of propofol on human amnion are rare. The current study investigated the effects of propofol on lipopolysaccharide (LPS)-induced inflammatory responses in human amnion-derived WISH cells.
Methods:WISH cells were exposed to LPS for 24 h and co-treated with various concentrations of propofol (0.01–1 μg/ml). Cell viability was measured using the MTT assay. Nitric oxide (NO) production was analyzed using a microassay based on the Griess reaction. The protein expression of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE 2), p38, and phospho-p38 was analyzed using western blotting.
Results:Propofol did not affect the viability and NO production of WISH cells. Co-treatment with LPS and propofol reduced COX-2 and PGE 2 protein expression and inhibited p38 phosphorylation in WISH cells.
Conclusion:Propofol does not affect the viability of WISH cells and inhibits LPS-induced expression of inflammatory factors. The inhibitory effect of propofol on inflammatory factor expression is likely mediated by the inhibition of p38 activation.