Involvement of prostaglandin transport system at the blood-brainbarrier in the drug-induced vascular disorder in the brain.

Research Project

Project/Area Number	20790127
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Medical pharmacy
Research Institution	Tohoku University
Principal Investigator	ITO Shingo Tohoku University, 大学院・薬学研究科, 助教 (20466535)
Project Period (FY)	2008 – 2009
Project Status	Completed (Fiscal Year 2009)
Budget Amount *help	¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000) Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2008: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Keywords	薬物動態学 / 血液脳関門 / プロスタグランディンE2 / 薬物相互作用 / プロスタグランディン / NSAIDs
Research Abstract	Using Brain Efflux Index method, prostaglandin E2 (PGE2) was eliminated from mouse brain with a half-life of 12 minutes. By contrast, PGE2 increased brain capillary endothelial cell proliferation and slightly recovered from NASIDs mediated cytotoxicity. These results demonstrate that BBB efflux transport system is involved in the PGE2 clearance in mouse brain and suggest that PGE2 stimulate vascularization and remodeling of brain capillary endothelial cells and NSAIDs itself exert significantly cytotoxicity against brain capillary endothelial cells. Therefore, NSAIDs mediated reduction of PGE2 clearance and cytotoxicity against brain capillary endothelial cells may cause severe angiopacy in brain inflammation.

Report

(3 results)