Project/Area Number |
25670042
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Pharmacology in pharmacy
|
Research Institution | Setsunan University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
YONEYAMA MASANORI 摂南大学, 薬学部, 准教授 (00411710)
芝 達雄 九州保健福祉大学, 薬学部, 助教 (00634958)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 難聴 / 酸化ストレス / ギャップ結合 / コネキシン / 内耳 / カルベノキソロン / 平衡感覚異常 / 薬理学 / 感音難聴 / 音響外傷ストレス / 心的ストレス / カルパイン |
Outline of Final Research Achievements |
Most of sensorineural hearing impairment has become a social problem, because there is no treatment of sensorineural hearing impairment. Under physiological conditions, maintenance of the potassium ion concentration in the endolymph by gap junction in the cochlear lateral wall is important for hearing. We found using in vivo and in vitro experiments that intense noise exposure produced disruption of gap junction through oxidative stress-induced connexin degradation prior to hair cell damage. Therefore, the collapse of ion balance in the inner ear through degradation of connexin is one of the causes of hair cell damages. In addition, calpain inhibitors prevented noise-induced hearing loss and disruption of gap junction induced by connexin degradation. Taken together, the disruption of gap junction by oxidative stress is involved in one of the pathogenesis of sensorineural hearing impairment and could be a new target of pharmacotherapy for sensorineural hearing impairment.
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