Disease control of MNU-induced animal models for retinitis pigmentosa by arachidonic acid and its molecular mechanisms

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592661
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Ophthalmology
• Research Institution: Kansai Medical University
• Principal Investigator: TSUBURA Airo 関西医科大学, 医学部, 教授 (90098137)
• 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)
• Project Period (FY): 2012-04-01 – 2015-03-31
• 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

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.

Free Research Field

実験病理学