Tissue Eng Regen Med.  2019 Jun;16(3):301-309. 10.1007/s13770-019-00194-y.

Propofol Suppresses LPS-Induced Inflammation in Amnion Cells via Inhibition of NF-κB Activation

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. anekej@pusan.ac.kr
  • 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-jB 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.

Keyword

Amnion; NF-κB; Inflammation; Preterm labor; Propofol

MeSH Terms

Amnion*
Anesthetics
Blotting, Western
Cyclooxygenase 2
Cytokines
Dinoprostone
Enzyme-Linked Immunosorbent Assay
Female
Humans
Inflammation*
NF-kappa B
Obstetric Labor, Premature
Perinatal Death
Pregnancy
Propofol*
Risk Factors
RNA, Messenger
Tumor Necrosis Factor-alpha
Anesthetics
Cyclooxygenase 2
Cytokines
Dinoprostone
NF-kappa B
Propofol
RNA, Messenger
Tumor Necrosis Factor-alpha
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