| Project/Area Number |
23500570
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Medical systems
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| Research Institution | Yokohama College of Pharmacy |
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Principal Investigator |
FUKAI Toshio 横浜薬科大学, 薬学部, 教授 (10057755)
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| Co-Investigator(Kenkyū-buntansha) |
YUMITA Nagahiko 横浜薬科大学, 薬学部, 教授 (40191481)
IWASE Yumiko 横浜薬科大学, 薬学部, 講師 (00521882)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | アポトーシス / 一重項酸素 / 活性酸素種 / 超音波 / 音響化学療法 |
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| Research Abstract |
Recently, we have been studying antitumor activation of porphyrin compounds by ultrasound. The present study aims to the application of sonodynamically inducted apoptosis by porphyrin compounds for cancer treatment. Cells treated with ultrasound and porphyrin sompounds such as Porfimer Sodium, ATX-70, ATX-S10, NPe6 and DCPH-Na clearly showed membrane blebbing and cell shrinkag. Also, DNA ladder formation and caspase-3 activation were pbserved in cells treated with ultrasound and porphyrin compounds but not in order treatments. In addition, the combination of porphyin compounds and ultrasound enhanced nitroxide generation measured by ESR. Sonodynamically induced apoptosis, caspase-3 activation, and nitroxide generation were significantly suppressed by histidine. These findings suggest that ultrasonically generated reactive oxygen species such as singlet oxygen is an important mediator of sonodynamically induced apoptosis.
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