2015 Fiscal Year Final Research Report
Mechanism of Shakuyaku-kannzo-to reduces paclitaxel-induced neuropathic pain
Project/Area Number |
24590325
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
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Research Institution | Fukushima Medical University |
Principal Investigator |
Kimura Junko 福島県立医科大学, 医学部, 教授 (10186322)
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Project Period (FY) |
2012-04-01 – 2016-03-31
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Keywords | 抗がん薬 / 芍薬甘草湯 / 神経痛 / T型Ca電流 / ホールセルクランプ法 / HEK293細胞 |
Outline of Final Research Achievements |
Paclitaxel is widely used for the treatment of solid malignant tumor, but its adverse effect is peripheral neuralgia. Shakuyaku-kanzo-to (SKT) is known to reduce pain of peripheral neuralgia induced by paclitaxel in mice. It was also reported that the voltage-dependent T-type Ca channels (Cav3.2 ) is involved in neuropathic pain. Therefore we investigated whether SKT inhibits T type Ca current using HEK cells expressing human T type Ca current (hCav3.2). We found that SKT inhibited T-type Ca current in HEK293 cells using the whole cell patch clamp method. SKT at 10 mg/ml completely inhibited the T type Ca current. The IC50 value of SKT was 1.3 mg/ml、and Hill coefficient was 1.1. Our result suggests that the inhibition of T-type Ca current may be involved in the analgesic effect of Shakuyaku-kanzo-to on paclitaxel-induced neuralgia.
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Free Research Field |
薬理学
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