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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
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Background: The primary aims of periodontal disease treatment is to remove dental plaque and calculus, the main causes of tooth loss, and restore periodontal tissue destroyed by inflammation. Periodontal disease treatment should also help maintain the alveolar bone, alleviate inflammation, and promote periodontal ligament cell proliferation, which is essential for tissue regeneration. Conventional antibiotics and anti-inflammatories have adverse side effects, especially during long-term use, so there is a need for adjunct treatment agents derived from natural products. The purpose of this study was to investigate whether the herbal flavone baicalein has the osteogenic activity under inflammatory conditions, and assess the involvement of osteoblast immediate early response 3 (IER3) expression. Methods: Human osteoblastic MG-63 cells were cultured with the pro-inflammatory cytokines tumor necrosis factor and interleukin 1 in the presence and absence of baicalein. Proliferation was assessed using the 3-[4,5-dimethylthiazol-2- yl]-2,5-diphenyltetrazolium bromide assay, and expression of IER3 mRNA was assessed using real-time polymerase chain reaction. The expression of IER3 protein levels and activation of associated signal transduction pathways were assessed using western blotting. Results: Baicalein increased IER3 mRNA and protein expression synergistically. In addition, baicalein reversed the suppression of cell proliferation, and the downregulation of osteogenic transcription factor runt-related transcription factor 2 and osterix induced by pro-inflammatory cytokines. Baicalein also upregulated the phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK 1/2). The upregulation of IER3 by pro-inflammatory cytokines was blocked by pretreatment with inhibitors of AKT, p38, JNK, and ERK 1/2. Conclusion: Baicalein mitigates the deleterious responses of osteoblasts to pro-inflammatory cytokines. Further, IER3 enhanced the effect of baicalein via activation of AKT, p38, JNK, and ERK pathways.
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참고문헌 (21)
참고문헌 신청
Bruce L Pihlstrom / 2005 / Periodontal diseases / The Lancet 366(9499):1809~1820
이상임 / 2015 / NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells / 치위생과학회지 15(6):753~760
Lars A. Christersson / 1987 / Tissue Localization of Actinobacillus actinomycetemcomitans in Human Periodontitis / Journal of Periodontology 58(8):529~539
G. Serino / 2001 / The effect of systemic antibiotics in the treatment of patients with recurrent periodontitis / Journal of Clinical Periodontology 28(5):411~418
Forner L / 2006 / Increased plasma levels of IL-6 in bacteremic periodontis patients after scaling / J Clin Periodontol 33:724~729
이상임 / 2015 / NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells / 치위생과학회지 15(6):753~760
Lars A. Christersson / 1987 / Tissue Localization of Actinobacillus actinomycetemcomitans in Human Periodontitis / Journal of Periodontology 58(8):529~539
G. Serino / 2001 / The effect of systemic antibiotics in the treatment of patients with recurrent periodontitis / Journal of Clinical Periodontology 28(5):411~418
Forner L / 2006 / Increased plasma levels of IL-6 in bacteremic periodontis patients after scaling / J Clin Periodontol 33:724~729
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