Simvastatin reduces myocardial infarct size via increased nitric oxide production in normocholesterolemic rabbits

Bao, Narentuoya; Ushikoshi, Hiroaki; Kobayashi, Hiroyuki; Yasuda, Shinji; Kawamura, Itta; Iwasa, Motoh; Yamaki, Takashi; Sumi, Shoichiro; Nagashima, Kenshi; Aoyama, Takuma; Kawasaki, Masanori; Nishigaki, Kazuhiko; Takemura, Genzou; Minatoguchi, Shinya

doi:10.1016/j.jjcc.2008.09.012

Cited by 16 publications

(16 citation statements)

References 22 publications

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“…Our findings revealed that the levels of EPC, SDF‐1α, VEGF, and NO were decreased greatly in the elderly patients with multivessel reocclusions compared to the elderly patients with one‐ or two‐vessel reocclusions. Oxidative stress responses and inflammatory responses decreased the overexpressions of EPC, SDF‐1α, VEGF, and NO, and the reduced circulating EPC, SDF‐1α, VEGF, and NO led to coronary in‐stent restenosis . The present study suggested that the decreased levels of EPC, SDF‐1α, VEGF, and NO were related to coronary in‐stent reocclusion and severity of reocclusion after coronary stenting and may be considered as the important targets for treatment in a new stent design for interventional therapy of coronary artery stenoses.…”

Section: Discussionmentioning

confidence: 51%

“…The oxidative stress also was associated with the production and activities of NO. Oxidative stress was inhibited by increasing NO levels, and the elevated NO levels remarkably decreased infarct size of myocardium …”

Section: Discussionmentioning

confidence: 99%

“…The coronary atherosclerosis accelerated thrombus formation which occluded the coronary arteries, and NO suppressed platelet activation pathways and thrombus formation. The study has found a clear link between damaged NO signaling pathways and myocardial infarction and it provided a novel promising therapy target in myocardial infarction …”

Section: Introductionmentioning

confidence: 99%

“…The study has found a clear link between damaged NO signaling pathways and myocardial infarction and it provided a novel promising therapy target in myocardial infarction. [16][17][18][19] Inflammation contributed to atherosclerosis and human atherosclerotic lesions showed a significant increase of inflammatory toll-like receptors expressions and the inflammatory toll-like receptors were the important determinants of the atherosclerosis. The toll-like receptor 2 (TLR2) promoted atherogenesis and atherosclerotic lesion progression.…”

Section: Introductionmentioning

confidence: 99%

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Oxidative stress and inflammation: Early predictive indicators of multiple recurrent coronary in‐stent chronic total occlusions in elderly patients after coronary stenting

Zhou

Guo

et al. 2020

IUBMB Life

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Pro‐inflammatory responses and oxidative stress damages, and effects of the reduced anti‐oxidation and anti‐inflammation were involved in development and progression of coronary heart disease. We tried to identify the effects of pro‐inflammatory and oxidative stress biomarkers as well as anti‐oxidant and anti‐inflammatory factors on multiple recurrent coronary in‐stent chronic total occlusions in elderly patients after coronary stenting. We determined the expression levels of endothelial progenitor cell (EPC), stromal cell‐derived factor‐1α (SDF‐1α), vascular endothelial growth factor (VEGF), nitric oxide (NO), toll‐like receptor 2 (TLR2), toll‐like receptor 3 (TLR3), toll‐like receptor 4 (TLR4), and soluble ST2 (sST2) in elderly patients with multiple recurrent coronary in‐stent chronic total occlusions after coronary stenting. The levels of EPC, SDF‐1α, VEGF, and NO were decreased in elderly patients with multiple recurrent coronary in‐stent chronic total occlusions (p < .001). The levels of TLR2, TLR3, TLR4, and sST2 were increased in elderly patients with multiple recurrent coronary in‐stent chronic total occlusions (p < .001). The oxidative stress damages and pro‐inflammatory responses played the crucial roles in multiple recurrent coronary in‐stent chronic total occlusions of elderly patients after coronary stent placement. The levels of TLR2, TLR3, TLR4, and sST2, and the expressions of EPC, SDF‐1α, VEGF, and NO could be considered as potential early predictive indicators for multiple recurrent coronary in‐stent chronic total occlusions in elderly patients after coronary stent implantation.

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Section: Discussionmentioning

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oxidative stress and inflammation: Early predictive indicators of multiple recurrent coronary in‐stent chronic total occlusions in elderly patients after coronary stenting

Zhou

Guo

et al. 2020

IUBMB Life

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“…Furthermore, simvastatin decreases severity of injury from an induced myocardial infarction (Bao et al. ) and improves postischemic ventricular function (Lefer et al. ).…”

Section: Introductionmentioning

confidence: 99%

Simvastatin mitigates increases in risk factors for and the occurrence of cardiac disease following 10 Gy total body irradiation

Lenarczyk

Haworth

et al. 2015

Pharmacology Res & Perspec

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The ability of simvastatin to mitigate the increases in risk factors for and the occurrence of cardiac disease after 10 Gy total body irradiation (TBI) was determined. This radiation dose is relevant to conditioning for stem cell transplantation and threats from radiological terrorism. Male rats received single dose TBI of 10 Gy. Age-matched, sham-irradiated rats served as controls. Lipid profile, heart and liver morphology and cardiac mechanical function were determined for up to 120 days after irradiation. TBI resulted in a sustained increase in total- and LDL-cholesterol (low-density lipoprotein-cholesterol), and triglycerides. Simvastatin (10 mg/kg body weight/day) administered continuously from 9 days after irradiation mitigated TBI-induced increases in total- and LDL-cholesterol and triglycerides, as well as liver injury. TBI resulted in cellular peri-arterial fibrosis, whereas control hearts had less collagen and fibrosis. Simvastatin mitigated these morphological injuries. TBI resulted in cardiac mechanical dysfunction. Simvastatin mitigated cardiac mechanical dysfunction 20–120 days following TBI. To determine whether simvastatin affects the ability of the heart to withstand stress after TBI, injury from myocardial ischemia/reperfusion was determined in vitro. TBI increased the severity of an induced myocardial infarction at 20 and 80 days after irradiation. Simvastatin mitigated the severity of this myocardial infarction at 20 and 80 days following TBI. It is concluded simvastatin mitigated the increases in risk factors for cardiac disease and the extent of cardiac disease following TBI. This statin may be developed as a medical countermeasure for the mitigation of radiation-induced cardiac disease.

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Pharmacological Preconditioning

Minatoguchi¹

2019

Cardioprotection Against Acute Myocardial Infarction

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Simvastatin reduces myocardial infarct size via increased nitric oxide production in normocholesterolemic rabbits

Abstract: Pre-ischemic treatment with simvastatin reduces MI size via NO production. Simvastatin could be a useful drug for coronary artery disease patients without dyslipidemia as it has direct protective effects.

Cited by 16 publications

References 22 publications

Oxidative stress and inflammation: Early predictive indicators of multiple recurrent coronary in‐stent chronic total occlusions in elderly patients after coronary stenting

Oxidative stress and inflammation: Early predictive indicators of multiple recurrent coronary in‐stent chronic total occlusions in elderly patients after coronary stenting

Simvastatin mitigates increases in risk factors for and the occurrence of cardiac disease following 10 Gy total body irradiation

Pharmacological Preconditioning

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