scholarly journals Garlic and Onion Attenuates Vascular Inflammation and Oxidative Stress in Fructose-Fed Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Marcela Alejandra Vazquez-Prieto ◽  
Cecilia Rodriguez Lanzi ◽  
Carina Lembo ◽  
Claudio Rómulo Galmarini ◽  
Roberto Miguel Miatello
Keyword(s):  
Oxidative Stress ◽  
Vascular Inflammation ◽  
Mesenteric Arteries ◽  
Male Wistar Rats ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Cell Adhesion Molecule 1 ◽  
Endothelial Nitric Oxide ◽  
New Evidence ◽  
And Oxidative Stress

This study evaluates the antioxidant and the anti-inflammatory properties of garlic (G) and onion (O) in fructose-fed rats (FFR). Thirty-day-old male Wistar rats were assigned to control (C), F (10% fructose in drinking water), F+T (tempol 1 mM as control antioxidant), F+G, and F+O. Aqueous G and O extracts were administered orally in doses of 150 and 400 mg/kg/d respectively, and along with tempol, were given during the last 8 weeks of a 14-week period. At the end of the study, FFR had developed insulin resistance, aortic NADPH oxidase activity, increased SBP, plasma TBARS and vascular cell adhesion molecule-1 (VCAM-1) expression in mesenteric arteries, and a decrease in heart endothelial nitric oxide synthase (eNOS). Garlic and onion administration to F rats reduced oxidative stress, increased eNOS activity, and also attenuated VCAM-1 expression. These results provide new evidence showing the anti-inflammatory and antioxidant effect of these vegetables.

scholarly journals GLP-1 Analog Liraglutide Improves Vascular Function in Polymicrobial Sepsis by Reduction of Oxidative Stress and Inflammation

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1175
Author(s):  
Johanna Helmstädter ◽  
Karin Keppeler ◽  
Franziska Aust ◽  
Leonie Küster ◽  
Katie Frenis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Function ◽  
Vascular Inflammation ◽  
Cecal Ligation ◽  
Isometric Tension ◽  
Polymicrobial Sepsis ◽  
Dot Blot ◽  
Markers Of Inflammation ◽  
Anti Inflammatory ◽  
And Oxidative Stress

Sepsis causes high mortality in the setting of septic shock. LEADER and other trials revealed cardioprotective and anti-inflammatory properties of glucagon-like peptide-1 (GLP-1) analogs like liraglutide (Lira). We previously demonstrated improved survival in lipopolysaccharide (LPS)-induced endotoxemia by inhibition of GLP-1 degradation. Here we investigate the effects of Lira in the polymicrobial sepsis model of cecal ligation and puncture (CLP). C57BL/6J mice were intraperitoneally injected with Lira (200 µg/kg/d; 3 days) and sepsis induced by CLP after one day of GLP-1 analog treatment. Survival and body temperature were monitored. Aortic vascular function (isometric tension recording), protein expression (immunohistochemistry and dot blot) and gene expression (qRT-PCR) were determined. Endothelium-dependent relaxation in the aorta was impaired by CLP and correlated with markers of inflammation (e.g., interleukin 6 and inducible nitric oxide synthase) and oxidative stress (e.g., 3-nitrotyrosine) was higher in septic mice, all of which was almost completely normalized by Lira therapy. We demonstrate that the GLP-1 analog Lira ameliorates sepsis-induced endothelial dysfunction by the reduction of vascular inflammation and oxidative stress. Accordingly, the findings suggest that the antioxidant and anti-inflammatory effects of GLP-1 analogs may be a valuable tool to protect the cardiovascular system from dysbalanced inflammation in polymicrobial sepsis.

scholarly journals Ac2-26 Alleviates Brain Injury after Cardiac Arrest and Cardiopulmonary Resuscitation in Rats via the eNOS Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Jing Gong ◽  
Qi-Hang Tai ◽  
Guang-Xiao Xu ◽  
Xue-Ting Wang ◽  
Jing-Li Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Brain Injury ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Saline Group ◽  
Related Factors ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
And Oxidative Stress

Background. Brain injury is the leading cause of death following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Ac2-26 and endothelial nitric oxide synthase (eNOS) have been shown to reduce neuroinflammation. This study is aimed at determining the mechanism by which Ac2-26 protects against inflammation during brain injury following CA and CPR. Methods. Sixty-four rats were randomized into sham, saline, Ac2-26, and Ac2-26+L-NIO (endothelial nitric oxide synthase (eNOS) inhibitor) groups. Rats received Ac2-26, Ac2-26+L-NIO, or saline after CPR. Neurologic function was assessed at baseline, 24, and 72 hours after CPR. At 72 hours after resuscitation, serum and brain tissues were collected. Results. Blood-brain barrier (BBB) permeability increased, and the number of surviving neurons and neurological function decreased in the saline group compared to the sham group. Anti-inflammatory and proinflammatory factors, neuron-specific enolase (NSE) levels, and the expression of eNOS, phosphorylated (p)-eNOS, inducible nitric oxide synthase (iNOS), and oxidative stress-related factors in the three CA groups significantly increased (P<0.05). BBB permeability decreased, and the number of surviving neurons and neurological function increased in the Ac2-26 group compared to the saline group (P<0.05). Ac2-26 increased anti-inflammatory and reduced proinflammatory markers, raised NSE levels, increased the expression of eNOS and p-eNOS, and reduced the expression of iNOS and oxidative stress-related factors compared to the saline group (P<0.05). The effect of Ac2-26 on brain injury was reversed by L-NIO (P<0.05). Conclusions. Ac2-26 reduced brain injury after CPR by inhibiting oxidative stress and neuroinflammation and protecting the BBB. The therapeutic effect of Ac2-26 on brain injury was largely dependent on the eNOS pathway.

scholarly journals Differential effects of eNOS uncoupling on conduit and small arteries in GTP-cyclohydrolase I-deficient hph-1 mice

2011 ◽  
Vol 301 (6) ◽  
pp. H2227-H2234 ◽  
Author(s):  
Livius V. d'Uscio ◽  
Leslie A. Smith ◽  
Zvonimir S. Katusic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Protein Expression ◽  
Endothelial Nitric Oxide Synthase ◽  
Mesenteric Arteries ◽  
Gtp Cyclohydrolase I ◽  
Small Arteries ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

In the present study, we used the hph-1 mouse, which displays GTP-cyclohydrolase I (GTPCH I) deficiency, to test the hypothesis that loss of tetrahydrobiopterin (BH4) in conduit and small arteries activates compensatory mechanisms designed to protect vascular wall from oxidative stress induced by uncoupling of endothelial nitric oxide synthase (eNOS). Both GTPCH I activity and BH4 levels were reduced in the aortas and small mesenteric arteries of hph-1 mice. However, the BH4-to-7,8-dihydrobiopterin ratio was significantly reduced only in hph-1 aortas. Furthermore, superoxide anion and 3-nitrotyrosine production were significantly enhanced in aortas but not in small mesenteric arteries of hph-1 mice. In contrast to the aorta, protein expression of copper- and zinc-containing superoxide dismutase (CuZnSOD) was significantly increased in small mesenteric arteries of hph-1 mice. Protein expression of catalase was increased in both aortas and small mesenteric arteries of hph-1 mice. Further analysis of endothelial nitric oxide synthase (eNOS)/cyclic guanosine monophosphate (cGMP) signaling demonstrated that protein expression of phosphorylated Ser1177-eNOS as well as basal cGMP levels and hydrogen peroxide was increased in hph-1 aortas. Increased production of hydrogen peroxide in hph-1 mice aortas appears to be the most likely mechanism responsible for phosphorylation of eNOS and elevation of cGMP. In contrast, upregulation of CuZnSOD and catalase in resistance arteries is sufficient to protect vascular tissue from increased production of reactive oxygen species generated by uncoupling of eNOS. The results of our study suggest that anatomical origin determines the ability of vessel wall to cope with oxidative stress induced by uncoupling of eNOS.

scholarly journals Perivascular Adipose Tissue as a Target for Antioxidant Therapy for Cardiovascular Complications

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 574 ◽  
Author(s):  
Andy W. C. Man ◽  
Yawen Zhou ◽  
Ning Xia ◽  
Huige Li
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Cardiovascular Diseases ◽  
Vascular Inflammation ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Cardiovascular Complications ◽  
Perivascular Adipose Tissue ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Vascular Oxidative Stress

Perivascular adipose tissue (PVAT) is the connective tissue surrounding most of the systemic blood vessels. PVAT is now recognized as an important endocrine tissue that maintains vascular homeostasis. Healthy PVAT has anticontractile, anti-inflammatory, and antioxidative roles. Vascular oxidative stress is an important pathophysiological event in cardiometabolic complications of obesity, type 2 diabetes, and hypertension. Accumulating data from both humans and experimental animal models suggests that PVAT dysfunction is potentially linked to cardiovascular diseases, and associated with augmented vascular inflammation, oxidative stress, and arterial remodeling. Reactive oxygen species produced from PVAT can be originated from mitochondria, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, and uncoupled endothelial nitric oxide synthase. PVAT can also sense vascular paracrine signals and response by secreting vasoactive adipokines. Therefore, PVAT may constitute a novel therapeutic target for the prevention and treatment of cardiovascular diseases. In this review, we summarize recent findings on PVAT functions, ROS production, and oxidative stress in different pathophysiological settings and discuss the potential antioxidant therapies for cardiovascular diseases by targeting PVAT.

Abstract P226: Endothelin-1 Overexpression Exaggerates Diabetes-induced Endothelial Dysfunction by Altering Oxidative Stress

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sofiane Ouerd ◽  
Noureddine Idris-Khodja ◽  
Muhammad O Mian ◽  
Jordan Gornitsky ◽  
Tlili Barhoumi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Mrna Expression ◽  
Vascular Complications ◽  
Mesenteric Arteries ◽  
Ros Production ◽  
Reverse Transcription Quantitative Pcr ◽  
Patients With Diabetes ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Objective: Increased endothelin (ET)-1 expression has been shown to cause endothelial dysfunction and oxidative stress. Plasma ET-1 is increased in patients with diabetes mellitus. Since endothelial dysfunction often precedes vascular complications in diabetes, we sought to determine whether ET-1 contributes to diabetes-induced endothelial dysfunction. We hypothesized that overexpression of ET-1 in the endothelium will exaggerate diabetes-induced endothelial dysfunction. Methods: Diabetes was induced by streptozotocin IP injections (STZ, 55 mg/kg/day) for 5 days in 6-week-old male wild-type (WT) mice and in mice overexpressing human ET-1 restricted to the endothelium (eET-1). Mice were studied 14 weeks later. Endothelial function and vascular remodeling using pressurized myography, reactive oxygen species (ROS) production by dihydroethidium staining and mRNA expression by reverse transcription-quantitative PCR were assessed in mesenteric arteries (MA). Results: MA endothelium-dependent vasodilatory responses to acetylcholine were reduced 24% by diabetes in WT (E max : 61±6 vs 84±3%, P <0.05), and further decreased by 12% in eET-1 (E max : 49±5, P <0.05). Diabetes decreased MA media/lumen in WT (2.4±0.1% vs 3.3±0.2%, P <0.05) and eET-1 (2.9±0.2% vs 4.0±0.2%, P <0.05), whereas ET-1 overexpression increased MA media/lumen to a similar extent in diabetic and non-diabetic WT mice ( P <0.05). Vascular ROS production in MA was increased 2-fold by diabetes in WT (5.0±0.5 vs 2.5±0.3 relative fluorescence units [RFU]/μm 2 , P <0.05) and further augmented 1.7-fold in eET-1 (8.5±1.2 RFU/μm 2 , P <0.05). Diabetes reduced endothelial nitric oxide synthase (eNOS, Nos3) mRNA expression in eET-1 by 50% (0.7±0.1 vs 1.4±0.2, P <0.05) but not in WT. Induction of diabetes caused a 50% increase in superoxide dismutase 1 ( Sod1 , 1.5±0.2 vs 1.0±0.0, P <0.05) and a 30% increase in Sod2 (1.3±0.1 vs 1.0±0.0, P <0.05) mRNA expression in WT but not in eET-1. Conclusions: Increased expression of ET-1 exaggerates diabetes-induced endothelial dysfunction. This may be caused by an increase in vascular oxidative stress, a decrease in eNOS expression and a decrease in antioxidant capacity.

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