Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells
김철홍, 이상훈, 윤지영, 김은정, 주종훈, 김연하, 최은지,
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김철홍 ( Kim Cheul-Hong ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
이상훈 ( Lee Sang-Hoon ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
윤지영 ( Yoon Ji-Young ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
김은정 ( Kim Eun-Jung ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
주종훈 ( Joo Jong-Hoon ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
김연하 ( Kim Yeon-Ha ) - Pusan National University Department of Integrated Biological Science
최은지 ( Choi Eun-Ji ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
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 PGE2 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.
키워드
Amnion; Inflammation; p38; Preterm Labor; Propofol
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