| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Research Abstract |
The present study was under gone to elucidate a role of nitric oxide (NO) on induction of facial palsy by inoculation of herpes simplex type 1 (HSV-1), and to evaluate the effects of edarabone to prevent occurrence of facial palsy of the viral origin. NO levels of in the facial nerve were measured by use of a high performance liquid chromatography and absorption photometry. Before the incidence of facial palsy, no substantial difference in NO levels was noted between HSV-1 inoculated sides (right) and the control (left) sides. When the facial nerve palsy occurred, NO levels of the paralyzed side were higher than of the other side. Following recovery of the palsy, NO of both sides were at the same level. In the mice that facial nerve paralysis did not occur in spite of inoculation of HSV-1, NO of both sides were at the same level. According to immunohistological study using the confocal laser microscope, inducible nitric oxide synthase (iNOS) was observed in the inflammatory cells at the geniculate ganglion in animals with facial palsy presents. It was recognized only at the involved paralyzed side not at the contralateral side. Edarabone, a free radical scavenger, was administed to the animals immediately after inoculation of HSV-1 for as long as 11 days. The results indicated that 10mg/kg of edarabone was effective in reducing the incidence of facial palsy. In conclusion, NO, which is supposed to be produced at the geniculate ganglion via iNOS, plays an important role in induction of facial palsy by HSV-1, and, such damages may be prevented by use of edarabone.
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