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Melatonin inhibits Prevotella intermedia lipopolysaccharide-induced production of nitric oxide and interleukin-6 in murine macrophages by suppressing NF-κB and STAT1 activity

Authors

  • Eun-Young Choi,

    1. Department of Biological Science, College of Medical and Life Sciences, Silla University, Busan, Korea
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  • Ji-Young Jin,

    1. Department of Biological Science, College of Medical and Life Sciences, Silla University, Busan, Korea
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  • Ju-Youn Lee,

    1. Department of Periodontology, School of Dentistry, Pusan National University, Yangsan, Gyeongsangnam-do, Korea
    2. Medical Research Institute, Pusan National University, Busan, Korea
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  • Jeom-Il Choi,

    1. Department of Periodontology, School of Dentistry, Pusan National University, Yangsan, Gyeongsangnam-do, Korea
    2. Medical Research Institute, Pusan National University, Busan, Korea
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  • In Soon Choi,

    1. Department of Biological Science, College of Medical and Life Sciences, Silla University, Busan, Korea
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  • Sung-Jo Kim

    1. Department of Periodontology, School of Dentistry, Pusan National University, Yangsan, Gyeongsangnam-do, Korea
    2. Medical Research Institute, Pusan National University, Busan, Korea
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Address reprint requests to Sung-Jo Kim, Department of Periodontology, School of Dentistry, Pusan National University, Beomeo-ri, Mulgeum-eup, Yangsan, Gyeongsangnam-do 626-870, Korea.
E-mail: sungjokim@pusan.ac.kr

Abstract

Abstract:  Although a range of biological and pharmacological activities of melatonin have been reported, little is known about its potential anti-inflammatory efficacy in periodontal disease. In this study, we investigated the effects of melatonin on the production of inflammatory mediators by murine macrophages stimulated with lipopolysaccharide (LPS) from Prevotella intermedia, a major cause of inflammatory reactions in the periodontium, and sought to determine the underlying mechanisms of action. Melatonin suppressed the production of nitric oxide (NO) and interleukin-6 (IL-6) at both gene transcription and translation levels in Pintermedia LPS-activated RAW264.7 cells. P. intermedia LPS-induced NF-κB-dependent luciferase activity was significantly inhibited by melatonin. Melatonin did not reduce NF-κB transcriptional activity at the level of IκB-α degradation. Melatonin blocked NF-κB signaling through the inhibition of nuclear translocation and DNA-binding activity of NF-κB p50 subunit and suppressed STAT1 signaling. Although further research is required to clarify the detailed mechanism of action, we conclude that melatonin may contribute to blockade of the host-destructive processes mediated by these two proinflammatory mediators and could be a highly efficient modulator of host response in the treatment of inflammatory periodontal disease.

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