Project/Area Number |
15K18922
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Medical pharmacy
|
Research Institution | Kyoto University (2016-2017) Kyushu University (2015) |
Principal Investigator |
Kajiwara Moto 京都大学, 医学研究科, 薬剤師(特定) (70645506)
|
Research Collaborator |
MASUDA Satohiro 九州大学, 病院薬剤部, 教授・薬剤部長
MATSUBARA Kazuo 京都大学, 医学部附属病院薬剤部, 教授・薬剤部長
NAKAGAWA Shunsaku 京都大学, 医学部附属病院薬剤部, 助教
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | トランスポーター / オキサリプラチン / 末梢神経障害 / 有機カチオントランスポーター / 後根神経節細胞 |
Outline of Final Research Achievements |
HEK293 cells transiently expressing human (h) or rat (r) oraganic cation transporter (OCT) were treated with oxaliplatin (L-OHP) and various concentrations of duloxetine (DLX). Lactate dehydrogenase activity and caspase activity induced by L-OHP was reduced by DLX treatment. Amount of Pt accumulated in cells was also decreased by DLX treatment. Those results suggested that DLX improved L-OHP induced peripheral neuropathy by interfering with L-OHP incorporation in dorsal root ganglion.
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