A investigation into anti-inflammatory effect of SK-0403 via DPP4-inhibition.
Project/Area Number |
25893149
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Research Category |
Grant-in-Aid for Research Activity Start-up
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Allocation Type | Single-year Grants |
Research Field |
Periodontology
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Research Institution | Kyushu University (2014) Hiroshima University (2013) |
Principal Investigator |
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Project Period (FY) |
2013-08-30 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 抗炎症効果 / DPP4阻害薬 / 肥満 / 脂肪細胞 / マクロファージ / 肝臓 / 糖尿病 / 脂肪 |
Outline of Final Research Achievements |
DPP-4 expression is reportedly increased in inflammatory disease patients, suggesting an association of DPP-4 with inflammation. In this study, first, lipopolysaccharide (LPS)-induced elevations of inflammatory cytokine mRNA expressions in RAW264.7 macrophages were shown to be significantly suppressed by co-incubation with a DPP-4 inhibitor, SK-0403, in the RAW264.7 cells. Regarding the molecular mechanism, LPS-induced NF-κB and AP-1 promoter activities were revealed to be suppressed by incubation with SK-0403. When 3T3-L1 and RAW cells were co-cultured and stimulated with LPS, the effects of SK-0403 on the suppression of cytokine expressions in 3T3-L1 adipocytes were more marked. Anti-inflammatory effects of SK-0403 were also observed in vivo on the elevated hepatic and adipose expressions and serum concentrations of inflammatory cytokines in association with the suppression of hepatic NF-κB transcriptional activity, in LPS-infused mice.
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Report
(3 results)
Research Products
(6 results)