scholarly journals Activation of CREB Protein With Tabersonine Attenuates STAT3 During Atherosclerosis in Apolipoprotein E-Deficient Mice

Dose-Response ◽  
2020 ◽  
Vol 18 (1) ◽  
pp. 155932582091206 ◽  
Author(s):  
Sen Shi ◽  
Li Song ◽  
Yong Liu ◽  
Yanzheng He
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Apolipoprotein E ◽  
Pathological Condition ◽  
Aortic Tissue ◽  
Altered Expression ◽  
Creb Protein ◽  
Treatment Groups ◽  
Mediators Of Inflammation ◽  
Deficient Mice

Objective: Atherosclerosis is a pathological condition of fat deposition in the arteries, which causes cardiovascular disorders. Management of atherosclerosis remains a challenge and conventional drugs used for its management have several limitations. This study evaluated the protective effect of tabersonine against atherosclerosis and assessed its molecular mechanism of action. Methods: Atherosclerosis was induced by feeding apolipoprotein E (ApoE)-deficient mice a high-fat diet. Mice were treated with 20 or 40 mg/kg of tabersonine intraperitoneally for the 12-week duration of the study. Atherosclerosis markers and nitric oxide were measured in the sera of ApoE-deficient mice. Mediators of inflammation and markers of oxidative stress were assessed using enzyme-linked immunosorbent assays. Western blotting, quantitative reverse transcriptase polymerase chain reaction, and immunohistochemistry analyses were conducted to determine the protein expression in aortic tissue. Results: The tabersonine-treatment groups had an improved lipid profile and enhanced liver function, compared to the ApoE treatment group. Tabersonine treatment resulted in reduced levels of nitric oxide, cytokines, and oxidative stress, compared to the ApoE group. The altered expression levels of protein inhibitor activated STAT-3 (PIAS3), signal transducer and activator of transcription-3 (STAT-3), and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα) in ApoE-deficient mice were ameliorated by tabersonine treatment. Moreover, cAMP-response-element-binding (CREB) expression was elevated in aortic tissue of tabersonine treatment groups, compared to the ApoE group. Conclusion: These results suggested that tabersonine ameliorates the expression of STAT-3 by activating CREB protein in atherosclerotic ApoE-deficient mice.

Prevention of Fatty Streak Formation of 17β-Estradiol Is Not Mediated by the Production of Nitric Oxide in Apolipoprotein E– Deficient Mice

Circulation ◽  
1997 ◽  
Vol 96 (9) ◽  
pp. 3048-3052 ◽  
Author(s):  
R. Elhage ◽  
F. Bayard ◽  
V. Richard ◽  
P. Holvoet ◽  
N. Duverger ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Apolipoprotein E ◽  
Fatty Streak ◽  
17Β Estradiol ◽  
Deficient Mice

Anti-atherosclerotic effect of housefly (Musca domestica) maggot-derived protein-enriched extracts by dampened oxidative stress in apolipoprotein E-deficient mice

RSC Advances ◽  
2016 ◽  
Vol 6 (107) ◽  
pp. 105363-105370 ◽  
Author(s):  
Xiao Mingzhu ◽  
Jin Xiaobao ◽  
Tang Futian ◽  
Wang Lijing ◽  
Mao Jianwen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Apolipoprotein E ◽  
Musca Domestica ◽  
Developed Countries ◽  
Morbidity And Mortality ◽  
Deficient Mice

Despitemany therapeutic advances, atherosclerosis remains the leading cause of morbidity and mortality in developed countries.

scholarly journals Absence of 12/15 Lipoxygenase Reduces Brain Oxidative Stress in Apolipoprotein E-Deficient Mice

2005 ◽  
Vol 167 (5) ◽  
pp. 1371-1377 ◽  
Author(s):  
Cinzia M. Chinnici ◽  
Yuemang Yao ◽  
Tao Ding ◽  
Colin D. Funk ◽  
Domenico Praticò
Keyword(s):  
Oxidative Stress ◽  
Apolipoprotein E ◽  
Brain Oxidative Stress ◽  
Deficient Mice

Abstract 276: Systemic Delivery of Microrna-146a Improves Endothelial Function and Ameliorates Atherosclerosis in Apolipoprotein E-deficient Mice

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Shuangtao Ma ◽  
Xiao Yu Tian ◽  
Chaofeng Mu ◽  
Haifa Shen ◽  
Yunrong Zhang ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Apolipoprotein E ◽  
Carotid Arteries ◽  
Treated Group ◽  
Vehicle Group ◽  
Early Event ◽  
Aortic Tissue ◽  
Systemic Delivery ◽  
Plaque Area ◽  
Deficient Mice

Rationale: Endothelial inflammation is an early event in the development of atherosclerosis. The microRNA (miR)-146a showed anti-inflammatory effects in cultured endothelial cells. In this study, we investigated the therapeutic role of miR-146a in endothelial function and atherosclerosis in apolipoprotein E (ApoE)-deficient mice. Methods and Results: The miR-146a was packaged into a multistage vector (MSV) that was conjugated with an E-selectin-targeting thioaptamer (ESTA) to form an ESTA-MSV microparticle. The ApoE-deficient mice were fed with Western diet and injected through tail vein with 15μg of miR-146a loaded ESTA-MSV microparticles or vehicle vectors biweekly for 12 weeks. The expressions of miR-146a in aortic tissue was increased by five times at two weeks after injection. However, the expressions of miR-146a in heart, lung, liver, spleen, kidney, and skeletal muscle were not increased. The acetylcholine-induced endothelium-dependent relaxations in both carotid arteries and aortas were significantly improved in mice from miR-146a treated group compared with vehicle group. In addition, the endothelium-dependent contractions of carotid arteries were also improved by miR-146a treatment. The en face oil red O staining of whole aortas showed the plaque area was decreased in miR-146a-treated mice. Application of miR-146a also decreased the plaque size, macrophages, and T-lymphocytes, but increased the collagen deposition and vascular smooth muscle cells in the sections of aortic roots. The PCR results showed that expressions of chemokine (C-C motif) ligand (CCL)-2, CCL-5, and CCL-8 were decreased by miR-146a. Conclusions: E-selectin-targeting delivery of miR-146a improves endothelial function and inhibits atherosclerosis.

scholarly journals Chronic iron overload intensifies atherosclerosis in apolipoprotein E deficient mice: Role of oxidative stress and endothelial dysfunction

Life Sciences ◽  
2019 ◽  
Vol 233 ◽  
pp. 116702 ◽  
Author(s):  
Vinícius Bermond Marques ◽  
Marcos André Soares Leal ◽  
Jandinay Gonzaga Alexandre Mageski ◽  
Helbert Gabriel Fidelis ◽  
Breno Valentim Nogueira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Iron Overload ◽  
Apolipoprotein E ◽  
Deficient Mice

IMPACT OF WESTERN TYPE DIET ON NITRIC OXIDE-MEDIATED RELAXATIONS IN THE AORTA OF APOLIPOPROTEIN E-DEFICIENT MICE

2004 ◽  
Vol 13 (3) ◽  
pp. 144
Author(s):  
Herta M Crauwels ◽  
Cor E Van Hove ◽  
Arnold G Herman ◽  
Hidde Bult
Keyword(s):  
Nitric Oxide ◽  
Apolipoprotein E ◽  
Deficient Mice

scholarly journals Nitric Oxide Synthetic Pathway in Patients with Microvascular Angina and Its Relations with Oxidative Stress

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Benedetta Porro ◽  
Sonia Eligini ◽  
Fabrizio Veglia ◽  
Alessandro Lualdi ◽  
Isabella Squellerio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Pathological Condition ◽  
No Synthase ◽  
Microvascular Angina ◽  
No Formation ◽  
Oxidative Stress Status ◽  
Patient Groups ◽  
Artery Disease ◽  
Reduced Forms

A decreased nitric oxide (NO) bioavailability and an increased oxidative stress play a pivotal role in different cardiovascular pathologies. As red blood cells (RBCs) participate in NO formation in the bloodstream, the aim of this study was to outline the metabolic profile of L-arginine (Arg)/NO pathway and of oxidative stress status in RBCs and in plasma of patients with microvascular angina (MVA), investigating similarities and differences with respect to coronary artery disease (CAD) patients or healthy controls (Ctrl). Analytes involved in Arg/NO pathway and the ratio of oxidized and reduced forms of glutathione were measured by LC-MS/MS. The arginase and the NO synthase (NOS) expression were evaluated by immunofluorescence staining. RBCs from MVA patients show increased levels of NO synthesis inhibitors, parallel to that found in plasma, and a reduction of NO synthase expression. When summary scores were computed, both patient groups were associated with a positive oxidative score and a negative NO score, with the CAD group located in a more extreme position with respect to Ctrl. This finding points out to an impairment of the capacity of RBCs to produce NO in a pathological condition characterized mostly by alterations at the microvascular bed with no significant coronary stenosis.

Sign in / Sign up

Export Citation Format

Share Document