Paclitaxel-Induced Endothelial Dysfunction in Living Rats Is Prevented by Nicorandil via Reduction of Oxidative Stress
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概要
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Paclitaxel-eluting stents dramatically reduce rates of in-stent restenosis; however, paclitaxel is known to lead to endothelial dysfunction. Protective effects of nicorandil on paclitaxel-induced endothelial dysfunction by examining flow-mediated dilation (FMD) were investigated in anesthetized rats. After 7-day osmotic infusion of paclitaxel (5 mg/kg per day), FMD was measured by high-resolution ultrasound in the femoral artery of living rats. Paclitaxel significantly reduced FMD (21.6% ± 3.2% to 7.1% ± 1.7%); this reduction was prevented by co-treatment with nicorandil (15 mg/kg per day), while paclitaxel did not affect nitroglycerin-induced vasodilation. Diazoxide and tempol, but not isosorbide dinitrate, had an effect similar to nicorandil in preventing paclitaxel-induced decrease in FMD. Nicorandil significantly prevented paclitaxel-induced reduction in acetylcholine-induced vasodilation. On the underling mechanisms, paclitaxel increased reactive oxygen species (ROS) production (dihydrorhodamine 123, DCF fluorescence intensity) and NADPH oxidase (p47<SUP>phox</SUP>, gp91<SUP>phox</SUP> mRNA) in arteries and human coronary artery endothelial cells (HCAECs), while paclitaxel reduced nitric oxide (NO) release (DAF-2 fluorescence intensity), but not endothelial NO synthase (eNOS) phosphorylation in HCAECs. Nicorandil prevented the increased ROS production in arteries and HCAECs, which was 5-hydroxydecanoate (5-HD)-sensitive but 1<I>H</I>-[1,2,4]oxadiazolo[4,3-<I>a</I>]quinoxalin-1-one (ODQ)-resistant, without significant effect on the reduced NO release. In conclusion, nicorandil prevents paclitaxel-induced endothelial dysfunction, which may be brought by improved NO bioavailability due to the reduction of oxidative stress via K<SUB>ATP</SUB> channel activation.
- 2012-08-20
著者
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Yogo Kenji
Product Research Department Chugai Pharmaceutical Co. Ltd.
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TAKAHARI Yoko
Teaching and Research Support Center, Tokai University School of Medicine
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SERIZAWA Ken-ichi
Product Research Department, Chugai Pharmaceutical Co., Ltd.
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Ishizuka Nobuhiko
Product Research Department Chugai Pharmaceutical Co. Ltd.
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Ishida Hideyuki
Department Of Digestive Tract And General Surgery Saitama Medical Center Saitama Medical University
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Serizawa Ken-ichi
Product Research Department Chugai Pharmaceutical Co. Ltd.
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Tashiro Yoshihito
Product Research Department Chugai Pharmaceutical Co. Ltd.
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Suzuki Toshihiko
Department Of Pediatrics Anjo Kosei Hospital
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Aizawa Ken
Product Research Department, Chugai Pharmaceutical Co., Ltd., Japan
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Sekine Kaori
Department of Pediatrics, Tokai University School of Medicine, Japan
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Yogo Kenji
Product Research Department, Chugai Pharmaceutical Co., Ltd.
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AIZAWA Ken
Product Research Department, Chugai Pharmaceutical Co., Ltd.
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SEKINE Kaori
Department of Pediatrics, Tokai University School of Medicine
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Ishida Hideyuki
Department of Chemistry, Faculty of Engineering Science, Osaka University
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