Naturally occurring anthocyanin cyanidin-3-rutinoside possesses inherent vasorelaxant actions and prevents methylglyoxal-induced vascular dysfunction in rat aorta and mesenteric arterial bed

2017 ◽  
Vol 95 ◽  
pp. 1251-1259 ◽  
Author(s):  
Thavaree Thilavech ◽  
Mahinda Y. Abeywardena ◽  
Michael Adams ◽  
Julie Dallimore ◽  
Sirichai Adisakwattana
Keyword(s):  
Vascular Dysfunction ◽  
Rat Aorta ◽  
Naturally Occurring ◽  
Mesenteric Arterial Bed

Diosgenin Mitigates Streptozotocin Diabetes-induced Vascular Dysfunction of the Rat Aorta

2015 ◽  
Vol 66 (6) ◽  
pp. 584-592 ◽  
Author(s):  
Farshad Roghani-Dehkordi ◽  
Mehrdad Roghani ◽  
Tourandokht Baluchnejadmojarad
Keyword(s):  
Vascular Dysfunction ◽  
Streptozotocin Diabetes ◽  
Rat Aorta

Omega-3E treatment regulates matrix metalloproteinases and prevents vascular reactivity alterations in diabetic rat aortaThis article is one of a selection of papers published in a special issue on Advances in Cardiovascular Research.

2009 ◽  
Vol 87 (12) ◽  
pp. 1063-1073 ◽  
Author(s):  
Esma N. Zeydanli ◽  
Belma Turan
Keyword(s):  
Matrix Metalloproteinases ◽  
Vascular Reactivity ◽  
Vascular System ◽  
Vascular Dysfunction ◽  
Vascular Complications ◽  
Close Correlation ◽  
Tissue Level ◽  
Rat Aorta ◽  
Diabetic Rat ◽  
Cardiovascular Research

It is known that increased generation of oxidants and (or) reduced endogenous antioxidant defense mechanisms are associated with the etiology of diabetic vascular complications. Although a close correlation exists between increased oxidative stress and the activation of matrix metalloproteinases (MMPs), little is known about the effect of hyperglycemia on the regulation and contribution of MMPs in the vascular system. Therefore, we aimed to examine whether omega-3E (50 mg/kg per day for 4 weeks), a long-chain (n-3) polyunsaturated fatty acid enriched with vitamin E, has a beneficial effect on vascular dysfunction via affecting MMPs in streptozotocin-diabetic rat aorta. Omega-3E treatment improved the diabetes-induced impairment of phenylephrine-induced contraction and isoproterenol-induced relaxation responses of aorta. It also exhibited marked protection against diabetes-induced degenerative changes in smooth muscle cell morphology. Biochemical data showed that this treatment significantly prevented important changes, such as inhibition of MMP-2 and MMP-9 activity, loss of tissue inhibitor of matrix metalloproteinase-4 (TIMP-4) protein, increase in tissue levels of thiol oxidation, endothelin-1, protein kinase C (PKC), and cAMP production, and decrease in tissue level of nitrite. These results indicated that omega-3E significantly improved impaired vascular responses and regulated the activity of MMPs via preventing oxidative injury. Overall, the data suggest that omega-3E ameliorates or prevents vascular reactivity alterations in diabetes. Such an observation provides preliminary evidence for omega-3E’s potential as a therapeutic agent for the prevention of vascular disorders in diabetes.

scholarly journals Modulatory Effect of 2-(4-Hydroxyphenyl)amino-1,4-naphthoquinone on Endothelial Vasodilation in Rat Aorta

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Javier Palacios ◽  
Fredi Cifuentes ◽  
Jaime A. Valderrama ◽  
Julio Benites ◽  
David Ríos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Calcium Release ◽  
Vascular Dysfunction ◽  
Rat Aorta ◽  
Cellular Mechanisms ◽  
No Donor ◽  
Pharmacological Agents ◽  
Naphthoquinone Derivative ◽  
Low Cytotoxicity ◽  
Endothelium Damage

The vascular endothelium plays an essential role in the control of the blood flow. Pharmacological agents like quinone (menadione) at various doses modulate this process in a variety of ways. In this study,Q7, a 2-phenylamino-1,4-naphthoquinone derivative, significantly increased oxidative stress and induced vascular dysfunction at concentrations that were not cytotoxic to endothelial or vascular smooth muscle cells.Q7reduced nitric oxide (NO) levels and endothelial vasodilation to acetylcholine in rat aorta. It also blunted the calcium release from intracellular stores by increasing the phenylephrine-induced vasoconstriction when CaCl2was added to a calcium-free medium but did not affect the influx of calcium from extracellular space.Q7increased the vasoconstriction to BaCl2(10−3 M), an inward rectifying K+channels blocker, and blocked the vasodilation to KCl (10−2 M) in aortic rings precontracted with BaCl2. This was recovered with sodium nitroprusside (10−8 M), a NO donor. In conclusion,Q7induced vasoconstriction was through a modulation of cellular mechanisms involving calcium fluxes through K+channels, and oxidative stress induced endothelium damage. These findings contribute to the characterization of new quinone derivatives with low cytotoxicity able to pharmacologically modulate vasodilation.

Chemerin reduces vascular nitric oxide/cGMP signalling in rat aorta: a link to vascular dysfunction in obesity?

2014 ◽  
Vol 127 (2) ◽  
pp. 111-122 ◽  
Author(s):  
Karla Bianca Neves ◽  
Núbia S. Lobato ◽  
Rhéure Alves Moreira Lopes ◽  
Fernando P. Filgueira ◽  
Camila Ziliotto Zanotto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Rat Aorta ◽  
Vascular Relaxation ◽  
Cgmp Signalling

The adipokine chemerin reduces NO/cGMP signalling in the vasculature contributing to decreased vascular relaxation.

IN VIVO ADMINISTRATION OF KETAMINE INHIBITS ENDOTOXIN-MEDIATED VASCULAR DYSFUNCTION IN RAT AORTA.

Shock ◽  
2003 ◽  
Vol 19 (Supplement) ◽  
pp. 39-40
Author(s):  
Leona J. Rubin ◽  
Lee Ann Newman ◽  
Hans D. Westermeyer ◽  
Shannon J. Kesting ◽  
John R. Dodam
Keyword(s):  
Vascular Dysfunction ◽  
Rat Aorta ◽  
In Vivo Administration

Chimeric SOD2/3 inhibits at the endothelial-neutrophil interface to limit vascular dysfunction in ischemia-reperfusion

2004 ◽  
Vol 287 (3) ◽  
pp. G676-G684 ◽  
Author(s):  
Claudine S. Bonder ◽  
Derrice Knight ◽  
Daniel Hernandez-Saavedra ◽  
Joe M. McCord ◽  
Paul Kubes
Keyword(s):  
Fusion Gene ◽  
Vascular Dysfunction ◽  
Ischemia Reperfusion ◽  
Microvascular Dysfunction ◽  
Proinflammatory Mediators ◽  
Naturally Occurring ◽  
Ischemic Episode ◽  
Reactive Oxidants ◽  
Positively Charged

After an ischemic episode, reperfusion causes profound oxidative stress in the vasculature of the afflicted tissue/organ. The dysregulated accumulation of reactive oxygen species (ROS), such as superoxide, has been closely linked to the production and release of proinflammatory mediators, a profound increase in adhesion molecule expression by the vascular endothelium, and infiltration of neutrophils during ischemia-reperfusion (I/R). Superoxide dismutase (SOD) has been shown to protect tissues and organs against I/R-induced injury; however, the drug had to be continuously perfused or kidneys had to be occluded to prevent clearance. We used intravital microscopy, a system that allowed us to visualize neutrophil-endothelial interactions within the mesenteric postcapillary venules of cats subjected to I/R and tested the hypothesis that I/R-induced neutrophil recruitment was inhibited by treatment with SOD2/3. SOD2/3 is a chimeric fusion gene product that contains the mature SOD2 as well as the COOH-terminal “tail” of SOD3 and, unlike the three naturally occurring SODs (SOD1, SOD2, and SOD3), which bear a net negative charge at pH 7.4, SOD2/3 is positively charged and physiologically stable. Our results suggest that not only does SOD2/3 have a much greater efficacy in vivo than the native human SOD2, but its administration prevents I/R-induced neutrophil-endothelial cell interactions and microvascular dysfunction. Moreover, our data support the hypothesis that reactive oxidants mediate I/R-induced injury and that the chimeric recombinant SOD2/3 has the potential to be a therapeutic agent against this debilitating illness.

High glucose causes vascular dysfunction through Akt/eNOS pathway: reciprocal modulation by juglone and resveratrol

2018 ◽  
Vol 96 (8) ◽  
pp. 757-764 ◽  
Author(s):  
M. Bilgehan Pektas ◽  
Ozge Turan ◽  
Gozde Ozturk Bingol ◽  
Esra Sumlu ◽  
Gökhan Sadi ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
High Glucose ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Vascular Dysfunction ◽  
Expression Profiles ◽  
Vascular Complications ◽  
Rat Aorta ◽  
High Fructose ◽  
Fructose 2

Transient elevations in blood glucose level may lead to changes in vascular function. Herein, we investigated the effects of high-glucose or high-fructose challenge, as well as potential influence of juglone or resveratrol on vascular reactivity, Akt/eNOS, and insulin signaling effectors in rat aorta. Aortic segments of rats were incubated with high glucose (30 mmol/L) or high fructose (2 mmol/L) in the absence and presence of juglone (5 μmol/L) or resveratrol (10 μmol/L). Acute high-glucose incubation markedly decreased acetylcholine-induced relaxation, which is further inhibited by juglone, but ameliorated by resveratrol. Incubation with high glucose caused significant reduction in pAkt/total Akt and peNOS/total eNOS ratios, as well as in the expression of some genes involved in insulin signaling. Juglone produced a further impairment, whereas resveratrol resulted in an improvement on the expression profiles of these proteins and genes. Acute exposure of aortic segments to high glucose causes a reduction in acetylcholine-induced relaxation in association with suppression of Akt/eNOS pathway, as well as several genes in insulin signaling pathway. Juglone and resveratrol have opposite actions on vascular relaxation and the above signaling targets. These findings could be relevant for the treatment of hyperglycemia-induced vascular complications.

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