2000 Fiscal Year Final Research Report Summary
Cytoprotection of prostaglandin under oxidative stress
| Project/Area Number |
11671739
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Shimane Medical University |
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Principal Investigator |
OHIRA Akihiro School of Medicine, Shimane Medical University, Professor, 医学部, 教授 (00169054)
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| Co-Investigator(Kenkyū-buntansha) |
TANE Nobuhiro School of Medicine, Shimane Medical University, Instractor, 医学部, 助手 (50277993)
TAKANASHI Taiji School of Medicine, Shimane Medical University, Assistant Professor, 医学部, 講師 (10226798)
SHIBUYA Yuzo School of Medicine, Shimane Medical University, Assistant Professor, 医学部, 講師 (20196455)
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| Project Period (FY) |
1999 – 2000
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| Keywords | Prostagurandin / Oxidative stress / Ischemia-reperfusion / Retina / Light damage / Redox |
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| Research Abstract |
Prostaglandin (PG) has various biological functions including breakdown of blood-retinal barrier and production of mediators in inflammations. Our previous study indicated that PG has release from oxidative stress, such as retinal ischemia/reperfusion and retinal photooxidation. We used the retinal light damage in rats, and observed the changes of cyclooxygenase-1 (Cox-1), Cox-2, PGE_2, PGD_2, and PGF_<2-> after light exposure. PGD_2 expression increased the photoreceptor outer segments after 24 hours. No changes were observed Cox-2, PGE_2, and PGF_<2-> after light exposure. We confirmed the increase of 8-hydroxy-deoxyguanosine (8-OhdG), one of the major DNA base-modified products, in the outer nuclear layaer during periods of light challenges. We examined the effect of N-acetylcysteine (NAC) in this project. NAC is one of exogenous thiol antioxidants. Increased level of thiols in cells or tissues associate with increased tolerance to oxidative stresses. NAC precluded the light induced diminishment of DNA damage of photoreceptor cells, suggesting that NAC restored light induced damage of photoreceptor cells. We observed decreased lipid peroxidation and thioredoxin upregulation, indicating that NAC attenuated oxidative stress. NAC administration attenuates the light induced photoreceptor cell damage via the suppression of oxidative stress, and manipulation of intracellular redox state may represent a useful therapeutic strategy.
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