Paclitaxel-Induced Endothelial Dysfunction in Living Rats Is Prevented by Nicorandil via Reduction of Oxidative Stress
endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species
Gespeichert in:
| Autor*in: |
Ken-ichi Serizawa [verfasserIn] Kenji Yogo [verfasserIn] Ken Aizawa [verfasserIn] Yoshihito Tashiro [verfasserIn] Yoko Takahari [verfasserIn] Kaori Sekine [verfasserIn] Toshihiko Suzuki [verfasserIn] Nobuhiko Ishizuka [verfasserIn] Hideyuki Ishida [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2012 |
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| Übergeordnetes Werk: |
In: Journal of Pharmacological Sciences - Elsevier, 2017, 119(2012), 4, Seite 349-358 |
|---|---|
| Übergeordnetes Werk: |
volume:119 ; year:2012 ; number:4 ; pages:349-358 |
| Links: |
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| DOI / URN: |
10.1254/jphs.12067FP |
|---|
| Katalog-ID: |
DOAJ047337591 |
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| 520 | |a 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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. Keywords:: endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species | ||
| 653 | 0 | |a Therapeutics. Pharmacology | |
| 700 | 0 | |a Kenji Yogo |e verfasserin |4 aut | |
| 700 | 0 | |a Ken Aizawa |e verfasserin |4 aut | |
| 700 | 0 | |a Yoshihito Tashiro |e verfasserin |4 aut | |
| 700 | 0 | |a Yoko Takahari |e verfasserin |4 aut | |
| 700 | 0 | |a Kaori Sekine |e verfasserin |4 aut | |
| 700 | 0 | |a Toshihiko Suzuki |e verfasserin |4 aut | |
| 700 | 0 | |a Nobuhiko Ishizuka |e verfasserin |4 aut | |
| 700 | 0 | |a Hideyuki Ishida |e verfasserin |4 aut | |
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10.1254/jphs.12067FP doi (DE-627)DOAJ047337591 (DE-599)DOAJ79dc6818431c4382858a22754ffa66be DE-627 ger DE-627 rakwb eng RM1-950 Ken-ichi Serizawa verfasserin aut Paclitaxel-Induced Endothelial Dysfunction in Living Rats Is Prevented by Nicorandil via Reduction of Oxidative Stress 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. Keywords:: endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species Therapeutics. Pharmacology Kenji Yogo verfasserin aut Ken Aizawa verfasserin aut Yoshihito Tashiro verfasserin aut Yoko Takahari verfasserin aut Kaori Sekine verfasserin aut Toshihiko Suzuki verfasserin aut Nobuhiko Ishizuka verfasserin aut Hideyuki Ishida verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 119(2012), 4, Seite 349-358 (DE-627)1760631620 13478613 nnns volume:119 year:2012 number:4 pages:349-358 https://doi.org/10.1254/jphs.12067FP kostenfrei https://doaj.org/article/79dc6818431c4382858a22754ffa66be kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319304797 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 119 2012 4 349-358 |
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10.1254/jphs.12067FP doi (DE-627)DOAJ047337591 (DE-599)DOAJ79dc6818431c4382858a22754ffa66be DE-627 ger DE-627 rakwb eng RM1-950 Ken-ichi Serizawa verfasserin aut Paclitaxel-Induced Endothelial Dysfunction in Living Rats Is Prevented by Nicorandil via Reduction of Oxidative Stress 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. Keywords:: endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species Therapeutics. Pharmacology Kenji Yogo verfasserin aut Ken Aizawa verfasserin aut Yoshihito Tashiro verfasserin aut Yoko Takahari verfasserin aut Kaori Sekine verfasserin aut Toshihiko Suzuki verfasserin aut Nobuhiko Ishizuka verfasserin aut Hideyuki Ishida verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 119(2012), 4, Seite 349-358 (DE-627)1760631620 13478613 nnns volume:119 year:2012 number:4 pages:349-358 https://doi.org/10.1254/jphs.12067FP kostenfrei https://doaj.org/article/79dc6818431c4382858a22754ffa66be kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319304797 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 119 2012 4 349-358 |
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10.1254/jphs.12067FP doi (DE-627)DOAJ047337591 (DE-599)DOAJ79dc6818431c4382858a22754ffa66be DE-627 ger DE-627 rakwb eng RM1-950 Ken-ichi Serizawa verfasserin aut Paclitaxel-Induced Endothelial Dysfunction in Living Rats Is Prevented by Nicorandil via Reduction of Oxidative Stress 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. Keywords:: endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species Therapeutics. Pharmacology Kenji Yogo verfasserin aut Ken Aizawa verfasserin aut Yoshihito Tashiro verfasserin aut Yoko Takahari verfasserin aut Kaori Sekine verfasserin aut Toshihiko Suzuki verfasserin aut Nobuhiko Ishizuka verfasserin aut Hideyuki Ishida verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 119(2012), 4, Seite 349-358 (DE-627)1760631620 13478613 nnns volume:119 year:2012 number:4 pages:349-358 https://doi.org/10.1254/jphs.12067FP kostenfrei https://doaj.org/article/79dc6818431c4382858a22754ffa66be kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319304797 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 119 2012 4 349-358 |
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10.1254/jphs.12067FP doi (DE-627)DOAJ047337591 (DE-599)DOAJ79dc6818431c4382858a22754ffa66be DE-627 ger DE-627 rakwb eng RM1-950 Ken-ichi Serizawa verfasserin aut Paclitaxel-Induced Endothelial Dysfunction in Living Rats Is Prevented by Nicorandil via Reduction of Oxidative Stress 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. Keywords:: endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species Therapeutics. Pharmacology Kenji Yogo verfasserin aut Ken Aizawa verfasserin aut Yoshihito Tashiro verfasserin aut Yoko Takahari verfasserin aut Kaori Sekine verfasserin aut Toshihiko Suzuki verfasserin aut Nobuhiko Ishizuka verfasserin aut Hideyuki Ishida verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 119(2012), 4, Seite 349-358 (DE-627)1760631620 13478613 nnns volume:119 year:2012 number:4 pages:349-358 https://doi.org/10.1254/jphs.12067FP kostenfrei https://doaj.org/article/79dc6818431c4382858a22754ffa66be kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319304797 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 119 2012 4 349-358 |
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10.1254/jphs.12067FP doi (DE-627)DOAJ047337591 (DE-599)DOAJ79dc6818431c4382858a22754ffa66be DE-627 ger DE-627 rakwb eng RM1-950 Ken-ichi Serizawa verfasserin aut Paclitaxel-Induced Endothelial Dysfunction in Living Rats Is Prevented by Nicorandil via Reduction of Oxidative Stress 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. Keywords:: endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species Therapeutics. Pharmacology Kenji Yogo verfasserin aut Ken Aizawa verfasserin aut Yoshihito Tashiro verfasserin aut Yoko Takahari verfasserin aut Kaori Sekine verfasserin aut Toshihiko Suzuki verfasserin aut Nobuhiko Ishizuka verfasserin aut Hideyuki Ishida verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 119(2012), 4, Seite 349-358 (DE-627)1760631620 13478613 nnns volume:119 year:2012 number:4 pages:349-358 https://doi.org/10.1254/jphs.12067FP kostenfrei https://doaj.org/article/79dc6818431c4382858a22754ffa66be kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319304797 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 119 2012 4 349-358 |
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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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. 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paclitaxel-induced endothelial dysfunction in living rats is prevented by nicorandil via reduction of oxidative stress |
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Paclitaxel-Induced Endothelial Dysfunction in Living Rats Is Prevented by Nicorandil via Reduction of Oxidative Stress |
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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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. Keywords:: endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species |
| abstractGer |
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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. Keywords:: endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species |
| abstract_unstemmed |
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 (p47phox, gp91phox 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 1H-[1,2,4]oxadiazolo[4,3-a]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 KATP channel activation. Keywords:: endothelial dysfunction, flow-mediated dilation, nicorandil, paclitaxel, reactive oxygen species |
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