| Project/Area Number |
24592661
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
TSUBURA Airo 関西医科大学, 医学部, 教授 (90098137)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIZAWA Katsuhiko 関西医科大学, 医学部, 講師 (70548396)
YURI Takashi 関西医科大学, 医学部, 講師 (50330212)
UEHARA Norihisa 関西医科大学, 医学部, 講師 (30368211)
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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 |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | アラキドン酸 / 網膜変性症 / 視細胞 / アポトーシス / ラット / MNU / 網膜色素変性症 / Retinitis pigmentosa / Arachidonic acid / Methylnitrosourea / Rat / Fatty acids / Apoptosis / TUNEL / Morphometry |
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| Outline of Final Research Achievements |
The effects of arachidonic acid (AA) on N-methyl-N-nitrosourea (MNU)-induced retinal degeneration was investigated in Lewis rats during the gestational, lactational and post-weaning periods. Dams were fed 0.1, 0.5 or 2.0% AA diets or a basal (< 0.01% AA) diet. On day 21, pups received 50 mg MNU/kg or vehicle, and were fed the same diet as their mother for 7 d. Retinal apoptosis was analyzed by the TUNEL assay 24 h after the MNU, and retinal morphology was examined 7 d post-MNU. Histologically, all rats that received MNU and were fed the basal and 0.1% AA diets developed photoreceptor cell loss in the central retina. The 0.5 and 2.0% AA diets rescued retinal damage. In parallel with the increase in serum and retinal AA levels, the apoptotic index in the central retina was dose-dependently decreased in rats fed the 0.5 and 2.0% AA diets. Therefore, an AA-rich diet rescued young Lewis rats from MNU-induced retinal degeneration via suppression of photoreceptor apoptosis.
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