Propofol Suppresses LPS-Induced Inflammation in Amnion Cells via Inhibition of NF-κB Activation
Authors: Yeon Ha Kim
Ji-Hye Ahn
Do-Wan Kim
Eun-Ji Choi
Eun-Jung Kim
Ji-Young Yoon
Moonjung Jeun
Journal: Tissue engineering and regenerative medicine (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Amnion; Inflammation; NF-κB; Preterm labor; Propofol.
Affiliations: 1Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute, Geumo-ro 20, Yangsan, Gyeongnam 50612 Republic of Korea., 2Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Geumo-ro 20, Yangsan, Gyeongnam 50612 Republic of Korea., 3Department of Integrated Biological Science, Pusan National University, 2 Busandaehak-ro 63beon-gil, Geumjeong-gu, Busan, 46241 Republic of Korea.

Abstract:  Background: Preterm labor is a leading risk factor for neonatal death and long-term impairment and linked closely with inflammation. Non-obstetric surgery is occasionally needed during pregnancy and the anesthetic drugs or surgery itself can give rise to inflammation. Here, we examined the influence of propofol pretreatment on the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) after lipopolysaccharide (LPS) stimulation. In addition, we evaluated the expression of pro-inflammatory cytokines and nuclear factor kappa B (NF-κB). Methods: Human amnion-derived WISH cells were used to investigate the effect of propofol on the LPS-induced expression of inflammatory substances involved in preterm labor. For the experiment, WISH cells were pretreated with various concentrations propofol (0.01-10 μg/ml) for 1 h and then treated with LPS (1 μg/ml) for 24 h. Cytotoxicity was evaluated using MTT assay. PGE2 concentration was assessed by ELISA. Protein expressions of COX-2, PGE2 and NF-κB were analyzed by western blotting analysis. RT-PCR was used for analysis of mRNA expression of COX-2, PGE2, interlukin (IL)-1β and tumor necrosis factor (TNF)-α. Results: Propofol showed no cytotoxicity on the WISH cells. LPS-induced PGE2 production and COX-2 and PGE2 expression were decreased after propofol pretreatment. Propofol also attenuated the LPS-induced mRNA expression of IL-1β and TNF-α. Moreover, the activation of NF-κB was inhibited by propofol pretreatment on LPS-stimulated WISH cells. Conclusion: We demonstrated that propofol suppresses the expression of inflammatory substances enhanced by LPS stimulation. Furthermore, this inhibitory effect of propofol on the inflammatory substance expression is mediated by suppression of NF-κB activation. 

Retracted: No

PubPeer comments:
 This paper makes use of * The establishment of a line (WISH) of human amnion cells was purchased from the American Type Culture Collection (ATCC CCL25TM, Manassas, VA, USA) * But as it is known since 1968 and confirmed in the 1980 s this is a HeLa contaminated cell line. How someone can still make use of WISH as a model of an amniotic cell line 53 years after it has been known to be contaminated is baffling. Furthermore the ATCC site where the authors have obtained this cell line makes this fact very clear by stating: *This line was originally thought to be derived from normal amnion, but was subsequently found, based on isoenzyme analysis, HeLa marker chromosomes, and DNA fingerprinting, to have been established via HeLa cell contamination.* The authors state * These results suggested that propofol exerts a protective effect on preterm labor induced by the inflammatory response. * But as WISH is not an amniotic cell line all the conclusions of this paper are invalid and this paper should be retracted. See the relevant [Cellosaurus entry] ,