Chronic treatment with polyethylene-glycolated superoxide dismutase partially restores endothelium-dependent vascular relaxations in cholesterol-fed rabbits.

Mügge, Andreas; Elwell, James H.; Peterson, Timothy E.; Hofmeyer, Timothy G.; Heistad, D D; Harrison, David G.

doi:10.1161/01.res.69.5.1293

Cited by 336 publications

(166 citation statements)

References 29 publications

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“…This condition would then inhibit the ultrastructural changes of aorta thus prevent the development of atherosclerotic lesion as shown in our study. The present study has shown that disrupted aortic ultrastructure has been improved in this finding, in line with previous study that showed endothelium injury impairment by ROS could be restored by antioxidants (Mugge et al, 1991). …”

Section: Electron Microscopic Observationsupporting

confidence: 93%

Hibiscus sabdariffa Linn. improves the aortic damage in diabetic rats by acting as antioxidant

Zainalabidin¹,

Budin²,

Anuar³

et al. 2018

J App Pharm Sci

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Chronic hyperglycaemia produces excessive free radicals which could lead to diabetic complications. Hibiscus sabdariffa Linn. is proven to have high antioxidant and antihyperlipidemic properties. The aim of the study was to investigate the effects of H. sabdariffa polyphenol-rich extract (HPE) in the aorta of diabetic rats. Twenty-four male rats were randomly divided into three groups, i.e. non-diabetes mellitus (NDM), diabetes mellitus (DM) and diabetes mellitus with HPE (DM + HPE). HPE at 100 mg/kg or saline as control vehicle were administered daily through oral gavage for 28 days prior to sacrification and the aorta was isolated for further analysis. The glucose level in DM + HPE was significantly lower compared to DM, indicating its potential as an antidiabetic agent. Conversely, catalase (CAT), superoxide dismutase (SOD) activity and the level of glutathione (GSH) in DM + HPE were significantly higher than DM. The level of malondialdehyde (MDA) and protein carbonyl were significantly lower in DM + HPE than DM. Lipid profile analysis demonstrated a significant decrease in triglyceride, total cholesterol and LDL-C in DM + HPE compared to DM, however, HDL-C was significantly increased. Microscopic observation showed a disrupted morphology of the thoracic aorta in diabetic rats. HPE may exert protective effects by acting as an antidiabetic, antihyperlipidemic and antioxidant agent to the thoracic aorta in diabetic rats.

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Section: Electron Microscopic Observationsupporting

confidence: 93%

Hibiscus sabdariffa Linn. improves the aortic damage in diabetic rats by acting as antioxidant

Zainalabidin¹,

Budin²,

Anuar³

et al. 2018

J App Pharm Sci

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“…Peroxynitrite may contribute to the pathogenesis of atherosclerosis by modifying LDL directly, as well as shown here by releasing copper from caeruloplasmin, which would then promote lipid peroxidation [17-l 91. Whether peroxynitrite is formed in the vasculature is still unclear, although indirect evidence supports the hypothesis that superoxide and nitric oxide are formed simultaneously in atherosclerotic lesions [20,21]. This study supports the idea that caeruloplasmin is a likely source of the redoxactive copper recently detected in atherosclerotic postmortem material [22], and this may have arisen as a consequence of direct damage by peroxynitrite.…”

Section: Freshly Taken Plasma (Heparinised) From Three Normalsupporting

confidence: 81%

Peroxynitrite releases copper from caeruloplasmin: implications for atherosclerosis

Swain¹,

Darley‐Usmar²,

Gutteridge³

1994

FEBS Letters

139

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Peroxynitrite may be formed in the vasculature by the reaction of superoxide with nitric oxide. When the blue copper-containing protein, caeruloplasmin, is incubated with peroxynitrite, copper is released, and ferroxidase activity and the blue colouration are lost. When plasma from normal subjects is incubated with peroxynitrite, the oxidant reacts with numerous plasma constituents but is still able to release copper from caeruloplasmin. As the ferroxidase activity of caeruloplasmin is lost in plasma in the presence of peroxynitrite, a second ferroxidase activity associated with peroxidised lipids, and not inhibited by azide, is formed.

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“…Additionally, hyperglycemia increases the production of ROS, of which SO Development 131 (10) Research article is known to combine with NO and deplete it from the system, thus inhibiting NO mediated intracellular signaling and downstream cellular responses (Mügge et al, 1991;Urbich et al, 2002;Zhang et al, 2001). The reaction between SO and NO is rapid, occurring at a rate of 6.7×10 9 M -1 s -1 , a near diffusion-limited rate (Huie and Padmajas, 1993).…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

et al. 2004

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Nitric oxide (NO) has been demonstrated to mediate events during ovulation,pregnancy, blastocyst invasion and preimplantation embryogenesis. However,less is known about the role of NO during postimplantation development. Therefore, in this study, we explored the effects of NO during vascular development of the murine yolk sac, which begins shortly after implantation. Establishment of the vitelline circulation is crucial for normal embryonic growth and development. Moreover, functional inactivation of the endodermal layer of the yolk sac by environmental insults or genetic manipulations during this period leads to embryonic defects/lethality, as this structure is vital for transport, metabolism and induction of vascular development. In this study, we describe the temporally/spatially regulated distribution of nitric oxide synthase (NOS) isoforms during the three stages of yolk sac vascular development (blood island formation, primary capillary plexus formation and vessel maturation/remodeling) and found NOS expression patterns were diametrically opposed. To pharmacologically manipulate vascular development,an established in vitro system of whole murine embryo culture was employed. During blood island formation, the endoderm produced NO and inhibition of NO(L-NMMA) at this stage resulted in developmental arrest at the primary plexus stage and vasculopathy. Furthermore, administration of a NO donor did not cause abnormal vascular development; however, exogenous NO correlated with increased eNOS and decreased iNOS protein levels. Additionally, a known environmental insult (high glucose) that produces reactive oxygen species(ROS) and induces vasculopathy also altered eNOS/iNOS distribution and induced NO production during yolk sac vascular development. However, administration of a NO donor rescued the high glucose induced vasculopathy, restored the eNOS/iNOS distribution and decreased ROS production. These data suggest that NO acts as an endoderm-derived factor that modulates normal yolk sac vascular development, and decreased NO bioavailability and NO-mediated sequela may underlie high glucose induced vasculopathy.

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Chronic treatment with polyethylene-glycolated superoxide dismutase partially restores endothelium-dependent vascular relaxations in cholesterol-fed rabbits.

Cited by 336 publications

References 29 publications

Hibiscus sabdariffa Linn. improves the aortic damage in diabetic rats by acting as antioxidant

Hibiscus sabdariffa Linn. improves the aortic damage in diabetic rats by acting as antioxidant

Peroxynitrite releases copper from caeruloplasmin: implications for atherosclerosis

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

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