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Dexmedetomidine and LPS co-treatment attenuates inflammatory response on WISH cells via inhibition of p38/NF-¥êB signaling pathway

Journal of Dental Anesthesia and Pain Medicine 2022³â 22±Ç 4È£ p.277 ~ 287
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±èżº ( Kim Tae-Sung ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
À±Áö¿µ ( Yoon Ji-Young ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
±èöȫ ( Kim Cheul-Hong ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
ÃÖÀºÁö ( Choi Eun-Ji ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
±è¿¬ÇÏ ( Kim Yeon-Ha ) - Pusan National University Department of Integrated Biological Science
±èÀºÁ¤ ( Kim Eun-Jung ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine

Abstract


Background: Inflammatory dental diseases that occur during pregnancy can cause preterm labor and/or intrauterine growth restriction. Therefore, proactive treatment of dental diseases is necessary during pregnancy. Dexmedetomidine (DEX) is a widely used sedative in the dental field, but research on the effect of DEX on pregnancy is currently insufficient. In this study, we investigated the effects of co-treatment with DEX and lipopolysaccharide (LPS) on inflammatory responses in human amnion-derived WISH cells.

Methods: Human amnion-derived WISH cells were treated with 0.001, 0.01, 0.1, and 1 ¥ìg/mL DEX with 1 ¥ìg/mL LPS for 24 h. Cytotoxicity of WISH cells was evaluated by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay. The protein expression of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), p38, and nuclear factor kappa B (NF-¥êB) was examined by western blot analysis. The mRNA expression of pro-inflammatory cytokines such as interleukin (IL)-1¥â and tumor necrosis factor (TNF)-¥á was analyzed by real-time quantitative polymerase chain reaction.

Results: Co-treatment with DEX and LPS showed no cytotoxicity in the WISH cells. The mRNA expression of IL-1¥â and TNF-¥á decreased after co-treatment with DEX and LPS. DEX and LPS co-treatment decreased the protein expression of COX-2, PGE2, phospho-p38, and phospho-NF-¥êB in WISH cells.

Conclusion: Co-treatment with DEX and LPS suppressed the expression of COX-2 and PGE2, as well as pro-inflammatory cytokines such as IL-1¥â and TNF-¥á in WISH cells. In addition, the anti-inflammatory effect of DEX and LPS co-treatment was mediated by the inhibition of p38/NF-¥êB activation.

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Cyclooxygenase 2 Inhibitors; Dexmedetomidine; Lipopolysaccharides; Prostaglandin E2; WISH Cells

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