Establishment of smoking animal model and understanding of the effect of smoking on the larynx
| Project/Area Number |
24791749
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Otorhinolaryngology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
UEHA RUMI 東京大学, 医学部附属病院, 助教 (10597131)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
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)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 喫煙 / 禁煙 / タバコ / 喉頭 / 炎症 / サイトカイン / 嗅覚 / 嗅細胞 / 酸化ストレス / 神経原性炎症 / TRP受容体 |
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| Outline of Final Research Achievements |
To figure out the mechanism of smoking effect on larynx pathophysiologically, we established how to make a smoking animal model (rats), using cigarette smoke solution, and then we examined mainly tissue alterations and changes in inflammatory cytokines.
By smoking,, mucosal epithelium became thickened, and increase of inflammatory cell infiltration, submucosal collagen fibers at the glottis, Ki67+ cells in the glottic mucosa, and hyperplasia of laryngeal glands were shown. These alterations improved by long-term smoking cessation. Additionally, though laryngeal gland secretion increased transiently, that was improved by long-term smoking cessation.
The results of RT- PCR analyses of inflammatory cytokines (TNF-α, IL-1β, IL-6, CD3e), Fibronectin1,and Osteopontin supported the organization changes in larynx.
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Report
(4 results)
Research Products
(4 results)
