| Project/Area Number |
24659060
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Environmental pharmacy
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| Research Institution | Fukuoka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SATHO Tomomitsu 福岡大学, 薬学部, 助教 (90369025)
IRIE Keiichi 福岡大学, 加齢脳科学研究所, 研究員 (50509669)
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| Research Collaborator |
HIRAMATSU Yukihiro 福岡大学, 大学院・薬学研究科, 大学院生
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 乳酸菌 / ゲノムDNA / 抗炎症作用 / toll-like receptor 9 / NF-κB / オリゴデオキシヌクレオチド / TLR9 / NF-kB |
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| Research Abstract |
The inhibition of chronic inflammation by long-term use of NSAIDs, an anti-inflammatory drug, leads to the prevention and treatment of cancer. However, NSAIDs induce gastrointestinal side effects. We therefore investigated genomic DNA, which is one of the anti-inflammatory components of lactic acid bacteria (LAB). The use of component allows the application of LAB for systemic tissues except for intestine. The present study showed that genomic DNA of LAB is taken up into Caco-2 cells, and toll-like receptor 9, a specific receptor of bacterial DNA, is one of the major pathways for the anti-inflammatory effects by genomic DNA of LAB. Since the mechanisms of anti-inflammatory effects differ between genomic DNA of LAB and NSAIDs, long-term use of genomic DNA of LAB may lead to the prevention and treatment of cancer without side effects.
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