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2002 Fiscal Year Final Research Report Summary

Molecular mechanism of anti-inflammatory action of leptin in periodontal disease

Research Project

Project/Area Number 13470386
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Morphological basic dentistry
Research InstitutionKyushu University

Principal Investigator

HANAZAWA Shigemas  Kyushu University Faculty of Dental Science, Prof, 歯学研究院, 教授 (60060258)

Co-Investigator(Kenkyū-buntansha) SHIOTA Susumu  Kyushu University Faculty of Dental Science. Asssit. Prof, 歯学研究院, 助手 (00150467)
SHIMOKAWA Osamu  Kyushu University Faculty of Dental Science. Assoc. Prof, 歯学研究院, 講師 (40136502)
Project Period (FY) 2001 – 2002
KeywordsLeptin / mMacrophage / LPS / Anti-inflammation / NF-κB
Research Abstract

Leptin is a key hormone-like cytokine of food intake and metabolism. Several studies have suggested that the hormone negatively regulates sensitivity of endotoxin shock and TNF-α toxicitity. We report here that leptin acts as a potent negative regulator of NF-κB, an important transcriptional factor in inflammatory responses. The hormone inhibited LPS-stimulated expression of COX-2 gene in J774 macrophage-like cells. The hormone inhibited the transcriptional activity of NF-κB via inhibitory action of phosphorylation and degradation of IκBα in LPS-treated cells. And also the entry to nuclear of p65 , a component of NF-κB, was inhibited by the hormone. Since the inhibitory effect of leptin on NF-κB was not observed in db/db mice, a mutant one that lacks leptin receptor, the inhibitory action is mediated through its receptor. NF-κB inhibition by the hormone contributed to negative regulation of prostaglandin biosythsis and TNF-α. These results demonstrate that leptin is a potent inhibitor of NF-κB signaling pathway and suggest that the hormone is a novel regulator in several inflammatory diseases.

  • Research Products

    (5 results)

All Other

All Publications (5 results)

  • [Publications] Ozaki K, Hanazawa S: "Porphyromonas gingivalis fimbriae inhibit caspase-3-mediated apoptosis of monocytic THP-1 cells under growth factor deprivation via extracellular signal-regulated kinase-dependent expression of p21 Cip/WAF1"Infection and Immunity. 69(8). 4944-5000 (2001)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Murakami Y., Hanazawa S.et al.: "A possible mechanism of maxillofacial abscess formation : involvement of Porphyromonas endodontalis lipopolysaccharide via the expression of inflammatory cytokines"Oral Microbiology and Immunology. 16(6). 321-325 (2001)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] 大森善弘, 花澤重正: "ペリオドンタルメデイスン"医歯薬出版株式会社. 318 (2001)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Ozaki K., Hanazawa S.: "Porphyromonas gingivalis fimbriae inhibit caspase-3-mediated apoptosis of monocytic THP-1 cells under growth factor deprivation via extracellular signal-regulated kinase-dependent expression of p21 Cip/WAF1"Infection and Immunity. 69(8). 4944-5000 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Murakami Y., Hanazawa S. et. al.: "A possible mechanism of maxillofacial abscess formation : involvement of Porphyromonas endodontaiis lipopolysaccharide via the expression of inflammatory cytokines"Oral Microbiology and Immunology. 16(6). 321-325 (2001)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 2004-04-14  

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