| Project/Area Number |
20590923
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Tottori University |
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Principal Investigator |
BURIOKA Naoto Tottori University, 医学部, 教授 (50252854)
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| Co-Investigator(Renkei-kenkyūsha) |
CHIKUMI Hiroki 鳥取大学, 医学部, 講師 (90283994)
SHIMIZU Eiji 鳥取大学, 医学部, 教授 (50187449)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 睡眠時無呼吸症候群 / 間歇的低酸素 / 時計遺伝子 / IL-6 / VEGF / 内科学 / 低酸素 / 生理学 |
|---|
| Research Abstract |
Obstructive sleep apnea syndrome (OSAS) clinically causes intermittent hypoxia (IH) during sleep. The levels of an inflammation cytokine interleukin-6 (IL-6) mRNA significantly elevated by IH condition in cultured human lung adenocarcinoma epithelial cells (A549), due to activation of the signaling pathway of nuclear factor-KB (NF-KB) which is a potent transcriptional activator of IL-6. However, the treatment of cells with IH had little effect on clock gene expressions. Serum concentrations of IL-6 in OSAS patients were significantly higher than in healthy subjects, but elevated levels of IL-6 in OSAS patients fell to the level of healthy subjects after CPAP therapy. The condition of IH can activate signal transduction to an inflammatory response, but not to circadian clock regulation. The increase of serum IL-6 may cause systemic inflammation in patients with OSAS.
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