Reactive oxygen species in saliva related acute myocardial infarction

The purpose of the present study was to evaluate whether endostatin overexpression could improve cardiac function, hemodynamics, and fibrosis in heart failure (HF) via inhibiting reactive oxygen species (ROS). The HF models were established by inducing ischemia myocardial infarction (MI) through ligation of the left anterior descending (LAD) artery in Sprague-Dawley (SD) rats. Endostatin level in serum was increased in MI rats. The decreases of cardiac function and hemodynamics in MI rats were enhanced by endostatin overexpression. Endostatin overexpression inhibited the increases of collagen I, collagen III, α-smooth muscle actin (SMA), connective tissue growth factor (CTGF), matrix metalloproteinase (MMP)-2 and MMP9 in the heart of MI rats. MI-induced cardiac hypertrophy was reduced by endostatin overexpression. The increased levels of malondialdehyde (MDA), superoxide anions, the promoted NAD(P)H oxidase (Nox) activity, and the reduced superoxide dismutase (SOD) activity in MI rats were reversed by endostatin overexpression. Nox4 overexpression inhibited the cardiac protective effects of endostatin. These results demonstrated that endostatin improved cardiac dysfunction and hemodynamics, and attenuated cardiac fibrosis and hypertrophy via inhibiting oxidative stress in MI-induced HF rats.

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d-Limonene Ameliorates Myocardial Infarction Injury by Reducing Reactive Oxygen Species and Cell Apoptosis in a Murine Model

Journal of Natural Products ◽

10.1021/acs.jnatprod.9b00523 ◽

2019 ◽

Vol 82 (11) ◽

pp. 3010-3019 ◽

Cited By ~ 5

Author(s):

Aimée Obolari Durço ◽

Diego Santos de Souza ◽

Luana Heimfarth ◽

Rodrigo Miguel-dos-Santos ◽

Thallita Kelly Rabelo ◽

...

Keyword(s):

Myocardial Infarction ◽

Reactive Oxygen Species ◽

Murine Model ◽

Cell Apoptosis ◽

Reactive Oxygen ◽

Oxygen Species

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Mesenchymal stem cells encapsulated in a reactive oxygen species-scavenging and O2-generating injectable hydrogel for myocardial infarction treatment

Chemical Engineering Journal ◽

10.1016/j.cej.2021.133511 ◽

2021 ◽

pp. 133511

Author(s):

Hao Ding ◽

Jie Ding ◽

Qingnian Liu ◽

Junxin Lin ◽

Mengying He ◽

...

Keyword(s):

Myocardial Infarction ◽

Reactive Oxygen Species ◽

Stem Cells ◽

Mesenchymal Stem Cells ◽

Reactive Oxygen ◽

Oxygen Species ◽

Injectable Hydrogel

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Reactive Oxygen Species Modulator-1 (ROMO-1) Polymorphism Rs6060566 and The Risk of Myocardial Infarction in Slovenian Subjects With Type 2 Diabetes Mellitus

10.21203/rs.3.rs-32757/v1 ◽

2020 ◽

Author(s):

Miha Tibaut ◽

Sara Mankoč Ramuš ◽

Daniel Petrovič

Keyword(s):

Diabetes Mellitus ◽

Myocardial Infarction ◽

Reactive Oxygen Species ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Coronary Artery ◽

Coronary Arteries ◽

Reactive Oxygen ◽

Oxygen Species

Abstract Background We aimed to examine the role of the rs6060566 polymorphism of the reactive oxygen species modulator-1 (ROMO-1) gene in the development of myocardial infarction (MI) in Caucasians with type 2 diabetes mellitus (T2DM). Methods A total of 1072 subjects with T2DM were enrolled in cross-sectional case-control study: 335 subjects with MI and 737 subjects without clinical signs of coronary artery disease (CAD). Genetic analysis of the rs6060566 polymorphism was performed in all subjects. To assess the degree of coronary artery obstruction, a subpopulation of 128 subjects with T2DM underwent coronary computed tomography (CT) angiography. Next, endarterectomy samples were obtained during myocardial revascularization from diffusely diseased coronary arteries in 40 cases, which were analysed for ROMO-1 expression according to their genotype. Results There were no statistically significant associations between different genotypes or alleles of the rs6060566 polymorphism and MI in subjects with T2DM. The carriers of the C allele of the ROMO-1 rs6060566 had a threefold increased likelihood of having coronary artery stenosis (AOR = 3.27, 95% CI 1.16–9.20). Furthermore, the carriers of the C allele showed higher number of positive cells for ROMO-1 expression in endarterectomy samples of coronary arteries. Conclusions In accordance to our study, the rs6060566 polymorphism of the ROMO-1 gene is not the risk factor for MI in Caucasians with T2DM. However, we found that subjects carrying the C allele were at a 3.27-fold increased risk of developing severe CAD compared with those who had nonobstructive CAD. Moreover, The C allele carriers showed statistically higher number of cells positive for ROMO-1 compared with T allele carriers in coronary endarterectomy samples.

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Effect of Natural Polyphenols on Reactive Oxygen Species in Patients with Myocardial Infarction: A Double Blind Placebo Controlled Trial

Journal of Medical Science And clinical Research ◽

10.18535/jmscr/v7i3.23 ◽

2019 ◽

Vol 7 (3) ◽

Author(s):

Dr Rahul Goyal ◽

Keyword(s):

Myocardial Infarction ◽

Reactive Oxygen Species ◽

Controlled Trial ◽

Reactive Oxygen ◽

Oxygen Species ◽

Double Blind ◽

Double Blind Placebo ◽

Natural Polyphenols

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N -Acetylcysteine Restores Isoflurane-induced Preconditioning against Myocardial Infarction during Hyperglycemia

Anesthesiology ◽

10.1097/00000542-200306000-00013 ◽

2003 ◽

Vol 98 (6) ◽

pp. 1384-1390 ◽

Cited By ~ 23

Author(s):

Franz Kehl ◽

John G. Krolikowski ◽

Dorothee Weihrauch ◽

Paul S. Pagel ◽

David C. Warltier ◽

...

Keyword(s):

Myocardial Infarction ◽

Reactive Oxygen Species ◽

Infarct Size ◽

Myocardial Infarct ◽

Reactive Oxygen ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Myocardial Infarct Size ◽

Oxygen Species ◽

Blood Glucose Concentrations

Background Hyperglycemia generates reactive oxygen species and prevents isoflurane-induced preconditioning. The authors tested the hypothesis that scavenging reactive oxygen species with N-acetylcysteine will restore protection against myocardial infarction produced by isoflurane in vivo. Methods Barbiturate-anesthetized dogs (n = 45) were instrumented for measurement of systemic hemodynamics. Myocardial infarct size and coronary collateral blood flow were measured with triphenyltetrazolium staining and radioactive microspheres, respectively. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion. Dogs were randomly assigned to receive an infusion of 0.9% saline or 15% dextrose in water to increase blood glucose concentrations to 600 mg/dl (hyperglycemia) in the absence or presence of isoflurane (1.0 minimum alveolar concentration) with or without pretreatment with N-acetylcysteine (150 mg/kg i.v.) in six experimental groups. Isoflurane was discontinued, and blood glucose concentrations were allowed to return to baseline values before left anterior descending coronary artery occlusion. Results Myocardial infarct size was 27 +/- 2% (n = 8) of the left ventricular area at risk in control experiments. Isoflurane significantly (P < 0.05) decreased infarct size (13 +/- 2%; n = 7). Hyperglycemia alone did not alter infarct size (29 +/- 3%; n = 7) but abolished the protective effect of isoflurane (25 +/- 2%; n = 8). N-Acetylcysteine alone did not affect infarct size (28 +/- 2%; n = 8) but restored isoflurane-induced cardioprotection during hyperglycemia (10 +/- 1%; n = 7). Conclusions Acute hyperglycemia abolishes reductions in myocardial infarct size produced by isoflurane, but N-acetylcysteine restores these beneficial effects. The results suggest that excessive quantities of reactive oxygen species generated during hyperglycemia impair isoflurane-induced preconditioning in dogs.

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