2005 Fiscal Year Final Research Report Summary
Effect of several drugs on disruption of blood-aqueous barrier
| Project/Area Number |
14571661
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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 | University of Toyama (2005)
Toyama Medical and Pharmaceutical University (2002-2004) |
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Principal Investigator |
HAYASAKA Seiji Univ of Toyama, Dept Ophthalmology, Professor, 医学部, 教授 (00004961)
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| Co-Investigator(Kenkyū-buntansha) |
ZHANG Xue-Yun Univ of Toyama, Dept Ophthalmology, Assistant, 医学部, 助手 (40324040)
HAYASAKA Yoriko Univ of Toyama, Dept Ophthalmology, Assistant, 医学部, 助手 (90334739)
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| Project Period (FY) |
2002 – 2005
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| Keywords | blood-aqueous barrier / aqueous flare / aqueous proteir / uvitis / corticosteroid / NSAID / cyclooxygenase / betaxolol |
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| Research Abstract |
Disruption of blood-aqueous barrier elevates protein and flare in the anterior chamber. PGE2,PGE2 receptor antagonist, and isopropyl unoprostone (PG-related antiglaucoma agent) disrupted the blood -aqueous barrier in pigmented rabbits. Betaxolol (antiglaucoma agent having calcium blocking activity), apraclonidine (α 2 agonist), epinephrine (β 2 antagonist), diviyefrin (β 2 antagonist), betamethasone (corticosteroid), fluorometholone (corticosteroid), diclofenac (non-steroidal anti-inflammatory drug), pranoprofen (non-steroidal anti-inflammatory drug), baicalein (a component isolated from medicinal herb), baicalin (a component isolated from medicinal herb), tramazoline (vasoconstructor), FR122047 (COX-1 inhibitor), and FR188582(COX-2 inhibitor) suppressed PGE2-induced aqueous, flare elevation in pigmented rabbits. Postoperative aqueous flare elevation was inhibited by Kakkon-to in cataract patients or by betaxolol in glaucoma patients. It is possible that these agents may be useful in treatment for uveitis.
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