<i>In vitro</i> effect of ascorbic acid on neutrophil–endothelial cell interaction

Jonas, Eleonore; Dwenger, A.; Hager, Anke

doi:10.1002/bio.1170080104

Cited by 27 publications

(2 citation statements)

References 14 publications

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“…Vitamin C (VC) (ascorbic acid) is a water-soluble antioxidant that directly scavenges ROS, like superoxide and hydroxyl radicals, hydrogen peroxide, singlet oxygen, and hypochlorous acid, and also guarantees the chain-breaking antioxidant action of vitamin E (VE) by reducing the VE radical to VE [17, 18]. In addition, VC has been shown to attenuate aspirin-induced gastric damage and to offer effective gastroprotection [19, 20].…”

Section: Introductionmentioning

confidence: 99%

Effects of Grape Seed Extract, Vitamin C, and Vitamin E on Ethanol- and Aspirin-Induced Ulcers

Cuevas

Calzado

Guerra

et al. 2011

Advances in Pharmacological Sciences

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Effects of GSE and vitamins C and E on aspirin- and ethanol-induced gastric ulcer and associated increases of lipid peroxidation in rats were compared. Two experiments were conducted. Rats were randomized into eight groups: a negative control and seven groups that received aspirin or ethanol for ulcer induction: one positive control (vehicle) and six with VC, VE, or GSE (25 and 250 mg/kg). Ulcer indexes and gastric levels of malondialdehyde (MDA) were quantified. VC, VE, and GSE (25 and 250 mg/kg) decreased aspirin, and ethanol-induced ulcers and MDA values compared with positive control group. The magnitude of aspirin ulcer reduction was comparable for all treatments, and MDA decrease with GSE was higher than with VC and tended to be greater, albeit none significantly, than with VE. GSE was more effective than VC and VE for lowering the ethanol ulcers, while the decrease of MDA levels with GSE was greater than with VC, but comparable to that achieved with VE. GSE protected against ethanol-induced gastric ulcers more effectively than VC or VE, while its protection against aspirin ulcers was comparable for all treatments. GSE produced the greatest reductions of gastric MDA in both models.

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Section: Introductionmentioning

confidence: 99%

Effects of Grape Seed Extract, Vitamin C, and Vitamin E on Ethanol- and Aspirin-Induced Ulcers

Cuevas

Calzado

Guerra

et al. 2011

Advances in Pharmacological Sciences

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“…Probucol and the antioxidant vitamins C and E have been demonstrated to slow the progression of atherosclerosis in laboratory animals (19,20) and to reduce cardiovascular mortality in large epidemiological surveys (21)(22)(23)(24). Among other biological effects, these antioxidant agents reduce leukocyte-endothelium interaction in response to various pathophysiological stimuli in vitro (25,26). It was thus the aim of the present study to investigate whether vitamins C and E, as well as the Food and Drug Administration-approved antioxidant drug probucol, can counteract CS-induced leukocyte activation/adhesion in the hamster.…”

mentioning

confidence: 99%

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

Lehr¹,

Frei²,

Arfors³

1994

Proc. Natl. Acad. Sci. U.S.A.

153

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A common feature of cigarette-smoke (CS)-associated diseases such as atherosclerosis and pulmonary emphysema is the activation, aggregation, and adhesion of leukocytes to micro-and macrovascular endothelium. A previous study, using a skinfold chamber model for intravial fluorescence microscopy in awake hamsters, has shown that exposure of hamsters to the smoke generated by one research cigarette elicits the adhesion of fluorescently labeled leukocytes to the endothelium of arterioles and small venules. By the combined use of intravital microscopy and scanning electron microscopy, we now demonstrate in the same animal model that (i) CS-induced leukocyte adhesion is not confined to the microcirculation, but that leukocytes also adhere singly and in clusters to the aortic endothelium; (ii) CS induces the formation in the bloodstream of aggregates between leukocytes and platelets; and (iii) CS-induced leukocyte adhesion to micro-and macrovascular endothelium and leukocyte-platelet aggregate formation are almost entirely prevented by dietary or intravenous pretreatment with the water-soluble antioxidant vitamin C (venules, 21.4 ± 11.0 vs. 149.6 ± 38.7 leukocytes per mm2, P < 0.01; arterioles, 8.5 ± 4.2 vs. 54.3 ± 21.6 leukocytes per mm2, P < 0.01; aortas, 0.8 ± 0.4 vs. 12.4 ± 5.6 leukocytes per mm2 P < 0.01; means ± SD of n = 7 animals, 15 min after CS exposure). No inhibitory effect was observed by pretreatment of the animals with the lipid-soluble antioxidants vitamin E or probucol. The protective effects of vitamin C on CSinduced leukocyte adhesion and aggregation were seen at vitamin C plasma levels (55.6 ± 22.2 spM, n 7) that can easily be reached in humans by dietary means or supplementation, suggesting that vitamin C effectively contributes to protection from CS-associated cardiovascular and pulmonary diseases in humans.Cigarette smoke (CS) has been identified as an independent major risk factor for the development of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease, emphysema, atherosclerosis, and coronary artery disease (1). Although the spectrum of adverse effects of CS involves multiple tissue and organ systems, a feature common to the pathomechanism of most CS-associated diseases is the activation and adhesion of circulating leukocytes to micro-and/or macrovascular endothelium (2-4), followed by acute and/or chronic leukocyte-mediated tissue damage (5, 6). In agreement with earlier reports on the sequestration and activation of leukocytes in the pulmonary microcirculation in rabbits (7), hamsters (8, 9), and humans (10), intravital microscopy in a skinfold chamber model in hamsters revealed that the exposure of hamsters to the smoke of one cigarette elicits the rolling and adhesion of fluorescently labeled leukocytes to the endothelium of small venules and arterioles in striated muscle (11). Leukocyte adhesion was significantly reduced by pretreatment of the animals with superoxide dismutase, implying a key mediator role for superoxide radicals in CS-induced leu...

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Chemiluminescence response and adherence of neutrophils to cultured endothelial cells–influence of immunoglobulin G

Jonas

Dwenger

Jonas

1995

J. Biolumin. Chemilumin.

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The effect of different concentrations (0.8, 4.35, 8.7, 17.5, 25 and 35 mg/mL) of intravenous immunoglobulin G (Endobulin) on neutrophil-endothelial cell interaction was studied using an in vitro model of human umbilical cord vein endothelial cells and human neutrophils. Because adherence of neutrophils to endothelial cells is an essential component in inflammatory processes leading to endothelial cell injury the influence of immunoglobulin G on adherence has been investigated. A second aim of the present study was to determine changes in chemiluminescence response of neutrophils during adherence to endothelial cells. Production of oxygen-derived metabolites, measured by chemiluminescence response of neutrophils, decreased significantly in the presence of 8.7 mg immunoglobulin/mL test during coincubation of neutrophils and endothelial cells (p < 0.025). The adherence of neutrophils to endothelial cells was significantly decreased at a concentration of 8.7 mg immunoglobulin/mL test (p < 0.025). The present results indicate that this preparation of immunoglobulin G might exert a protective effect on neutrophil-endothelial cell interaction by decreasing adherence of neutrophils to endothelial cells and by scavenging reactive oxygen metabolites. metabolites. Therefore, the current investigation points to a probable protective effect of immunoglobulin G in oxidative diseases, such as the adult respiratory distress syndrome.

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In vitro effect of ascorbic acid on neutrophil–endothelial cell interaction

Cited by 27 publications

References 14 publications

Effects of Grape Seed Extract, Vitamin C, and Vitamin E on Ethanol- and Aspirin-Induced Ulcers

Effects of Grape Seed Extract, Vitamin C, and Vitamin E on Ethanol- and Aspirin-Induced Ulcers

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

Chemiluminescence response and adherence of neutrophils to cultured endothelial cells–influence of immunoglobulin G

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