Journal of Dental Anesthesia and Pain Medicine

The Korean Dental Society of Anesthsiology (대한치과마취과학회)
권호 표지
DOI QR코드

DOI QR Code

Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells

  • Kim, Cheul-Hong (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) ;
  • Lee, Sang-Hoon (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) ;
  • Yoon, Ji-Young (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) ;
  • Kim, Eun-Jung (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) ;
  • Joo, Jong Hoon (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) ;
  • Kim, Yeon Ha (Department of Integrated Biological Science, Pusan National University) ;
  • Choi, Eun-Ji (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute)
  • Received : 2022.07.07
  • Accepted : 2022.09.14
  • Published : 2022.10.01
Download PDF
⟨ Previous Next ⟩

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 ㎍/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.

Keywords

Acknowledgement

This work was supported by a 2-Year Research Grant from the Pusan National University.

References

  1. Ansari A, Bose S, You Y, Park S, Kim Y. Molecular mechanism of microbiota metabolites in preterm birth: pathological and therapeutic insights. Int J Mol Sci 2021; 22: 8145. https://doi.org/10.3390/ijms22158145
  2. Boyle AK, Rinaldi SF, Norman JE, Stock SJ. Preterm birth: inflammation, fetal injury and treatment strategies. J Reprod Immunol 2016; 119: 62-6. https://doi.org/10.1016/j.jri.2016.11.008
  3. Cappelletti M, Della Bella S, Ferrazzi E, Mavilio D, Divanovic S. Inflammation and preterm birth. J Leukoc Biol 2016; 99: 67-78. https://doi.org/10.1189/jlb.3MR0615-272RR
  4. Dixon CL, Richardson L, Sheller-Miller S, Saade G, Menon R. A distinct mechanism of senescence activation in amnion epithelial cells by infection, inflammation, and oxidative stress. Am J Reprod Immunol 2018; 79: e12790. https://doi.org/10.1111/aji.12790
  5. Komine-Aizawa S, Aizawa S, Hayakawa S. Periodontal diseases and adverse pregnancy outcomes. J Obstet Gynaecol Res 2019; 45: 5-12. https://doi.org/10.1111/jog.13782
  6. Tolcher MC, Fisher WE, Clark SL. Nonobstetric surgery during pregnancy. Obstet Gynecol 2018; 132: 395-403. https://doi.org/10.1097/AOG.0000000000002748
  7. Trahan MJ, Nicholls-Dempsey L, Richardson K, Wou K. Ludwig's angina in pregnancy: a case report. J Obstet Gynaecol Can 2020; 42: 1267-70. https://doi.org/10.1016/j.jogc.2020.03.014
  8. Nie Y, Lu YX, Lv LH. Effect of propofol on generation of inflammatory mediator of monocytes. Asian Pac J Trop Med 2015; 8: 964-70. https://doi.org/10.1016/j.apjtm.2015.10.008
  9. Pavan B, Fiorini S, Ferretti ME, Vesce F, Biondi C. WISH cells as a model for the "in vitro" study of amnion pathophysiology. Curr Drug Targets Immune Endocr Metabol Disord 2003; 3: 85-94.
  10. He MT, Park HS, Kim YS, Lee AY, Cho EJ. Protective effect of membrane-free stem cells against lipopoly-saccharide and interferon-gamma-stimulated inflammatory responses in RAW 264.7 macrophages. Int J Mol Sci 2021; 22: 6894. https://doi.org/10.3390/ijms22136894
  11. Pasare C, Medzhitov R. Toll-like receptors: linking innate and adaptive immunity. Microbes Infect 2004; 6: 1382-7. https://doi.org/10.1016/j.micinf.2004.08.018
  12. Cho W, Choe J. Prostaglandin E2 stimulates COX-2 expression via mitogen-activated protein kinase p38 but not ERK in human follicular dendritic cell-like cells. BMC Immunol 2020; 21: 20. https://doi.org/10.1186/s12865-020-00347-y
  13. Ledingham MA, Thomson AJ, Greer IA, Norman JE. Nitric oxide in parturition. BJOG 2000; 107: 581-93. https://doi.org/10.1111/j.1471-0528.2000.tb13297.x
  14. Yallampalli C, Dong YL, Gangula PR, Fang L. Role and regulation of nitric oxide in the uterus during pregnancy and parturition. J Soc Gynecol Investig 1998; 5: 58-67. https://doi.org/10.1016/S1071-5576(97)00106-8
  15. Yoon JY, Kim DW, Ahn JH, Choi EJ, Kim YH, Jeun M, et al. Propofol suppresses LPS-induced inflammation in amnion cells via inhibition of NF-κB activation. Tissue Eng Regen Med 2019; 16: 301-9. https://doi.org/10.1007/s13770-019-00194-y
  16. Inada T, Kubo K, Kambara T, Shingu K. Propofol inhibits cyclo-oxygenase activity in human monocytic THP-1 cells. Can J Anaesth 2009; 56: 222-9. https://doi.org/10.1007/s12630-008-9035-0
  17. Kim JD, Ahn BM, Joo BS, Kwon JY, Chung HJ, Yu SB. Effect of propofol on prostaglandin E2 production and prostaglandin synthase-2 and cyclooxygenase-2 expressions in amniotic membrane cells. J Anesth 2014; 28: 911-8. https://doi.org/10.1007/s00540-014-1830-x
  18. Duchesne MJ, Thaler-Dao H, de Paulet AC. Prostaglandin synthesis in human placenta and fetal membranes. Prostaglandins 1978; 15: 19-42. https://doi.org/10.1016/S0090-6980(78)80003-3
  19. Challis JR, Sloboda DM, Alfaidy N, Lye SJ, Gibb W, Patel FA, et al. Prostaglandins and mechanisms of preterm birth. Reproduction 2002; 124: 1-17. https://doi.org/10.1530/reprod/124.1.1
  20. Wei L, Matsumoto H, Yamaguchi H. Propofol attenuates lipopolysaccharide-induced monocyte chemoattractant protein-1 production through p38 MAPK and SAPK/JNK in alveolar epithelial cells. J Anesth 2013; 27: 366-73. https://doi.org/10.1007/s00540-012-1539-7
  21. Pua LJW, Mai CW, Chung FF, Khoo AS, Leong CO, Lim WM, et al. Functional roles of JNK and p38 MAPK signaling in nasopharyngeal carcinoma. Int J Mol Sci 2022; 23: 1108. https://doi.org/10.3390/ijms23031108
  22. Li Z, Dai A, Yang M, Chen S, Deng Z, Li L. p38MAPK signaling pathway in osteoarthritis: pathological and therapeutic aspects. J Inflamm Res 2022; 15: 723-34. https://doi.org/10.2147/JIR.S348491
  23. Tang J, Hu JJ, Lu CH, Liang JN, Xiao JF, Liu YT, et al. Propofol inhibits lipopolysaccharide-induced tumor necrosis factor-alpha expression and myocardial depression through decreasing the generation of superoxide anion in cardiomyocytes. Oxid Med Cell Longev 2014; 2014: 157376. https://doi.org/10.1155/2014/157376
  24. Tang J, Chen X, Tu W, Guo Y, Zhao Z, Xue Q, et al. Propofol inhibits the activation of p38 through up-regulating the expression of annexin A1 to exert its anti-inflammation effect. PLoS One 2011; 6: e27890. https://doi.org/10.1371/journal.pone.0027890