| Budget Amount *help |
¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 2004: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2003: ¥3,100,000 (Direct Cost: ¥3,100,000)
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| Research Abstract |
The aim of this study is to investigate the effects of free radicals (NO,ROS) and apoptosis to the inner ear disorders and to develop the new treatments for the inner ear disease by modulating and/or inhibiting the various steps of the mechanisms of inner ear disorders.
As a result, certain stimuli induce the formation of free radicals, such as NO,ROS, resulting in a damage of inner ear. Subsequently, the sensory cells began to death by apoptosis. Calpain and caspase may play an important role for the apoptosis. These mechanisms were suggested to be a common pathway for almost all inner ear disorders. Based on these results, we investigated the attenuation of inner ear disorders by scavenging free radicals, inhibition of caspase or calpain and the addition of neurotrophines. All drugs used limited the hair cell damage and the combinations of drugs, such as inhibition of free radicals + neurotrophine, inhibition of free radicals + calpain or caspase inhibitors, had a significantly stronger preventive effect on hair cell damage. Based on these basic research, we have applied radical scavengers (rebamipide, vitamin C, glutathione) to the poor controlled Meniere's disease, cisplatin ototoxicity and presbyacusis. The results of these clinical trials are sufficient revealing an improvement of hearing.
These results were presented at the meetings (13th and 14th meeting of the Otological Society of Japan, 62th and 63th meeting of Japan Society for Equilibrium Reseach, 40th Workshop on Inner Ear Biology) and were presented by 10 papers
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