Additional Antilipoperoxidant Activities of Alpha-Tocopherol and Ascorbic Acid on Membrane-Like Systems Are Potentiated by Rutin

Nègre-Salvayre, A.N.; Affany, A.; Hariton, C.; Salvayre, Robert

doi:10.1159/000138807

Cited by 70 publications

(38 citation statements)

References 19 publications

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“…Ascorbate was found to be stimulatory, rather than inhibitory, which could be explained by the observation that under certain conditions ascorbate functions as a pro-oxidant, rather than an antioxidant, possibly due to the ability of ascorbic acid to release transitional metal ions from protein complexes leading to the generation of free radicals (71)(72)(73)(74)(75)(76)(77). Ascorbic acid has been shown to protect a-tcp from oxidation and in doing so enhance the latter's antioxidant activity (78)(79)(80). In our studies the addition of ascorbate plus a-tcp led to no net effect on agonistinduced monocyte adhesion, which suggests the possibility that the a-tcp reduced the enhancement in IL-1-induced adhesion caused by ascorbate alone.…”

Section: Effect Of A-tcp On Ec Expression Of E-selectin It Has Beenmentioning

confidence: 99%

Alpha-tocopherol inhibits agonist-induced monocytic cell adhesion to cultured human endothelial cells.

Faruqi¹,

Motte²,

DiCorleto³

1994

J. Clin. Invest.

210

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Antioxidants have been proposed to be anti-atherosclerotic agents; however, the mechanisms underlying their beneficial effects are poorly understood. We have examined the effect of a-tocopherol (a-tcp) on one cellular event in atherosclerotic plaque development, monocyte adhesion to stimulated endothelial cells (ECs). Human umbilical vein ECs were pretreated with a-tcp before stimulation with known agonists of monocyte adhesion: IL-1 (10 ng/ml), LPS (10 ng/ ml), thrombin (30 U/ml), or PMA (10 nM). Agonist-induced monocytic cell adhesion, but not basal adhesion, was inhibited in a time-and concentration-dependent manner by atcp. The IC50 of a-tcp on an IL-i-induced response was 45 jpM. The inhibition correlated with a decrease in steady state levels of E-selectin mRNA and cell surface expression of E-selectin which is consistent with the ability of a monoclonal antibody to E-selectin to inhibit monocytic cell adhesion in this system. Probucol (50 ,uM) and N-acetylcysteine (20 mM) also inhibited agonist-induced monocytic cell adhesion; whereas, several other antioxidants had no significant effect. Protein kinase C (PKC) does not appear to play a role in the a-tcp effect since no suppression of phosphorylation of PKC substrates was observed. Activation of the transcription factor NF-cB is reported to be necessary but not sufficient for E-selectin expression in EC. Electrophoretic mobility shift assays failed to show an cr-tcp-induced decrease in activation of this transcription factor after cytokine stimulation. It has been hypothesized that ca-tcp acts as an anti-atherosclerotic molecule by inhibiting generation of oxidized LDL-a putative triggering molecule in the atherosclerotic process. Our results point to a novel alternative mechanism of action of a-tcp. (J. Clin. Invest. 1994. 94:592-600.)

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Section: Effect Of A-tcp On Ec Expression Of E-selectin It Has Beenmentioning

confidence: 99%

Alpha-tocopherol inhibits agonist-induced monocytic cell adhesion to cultured human endothelial cells.

Faruqi¹,

Motte²,

DiCorleto³

1994

J. Clin. Invest.

210

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“…30 Rutin is an important antilipoperoxidant agent and has been found to be a strong scavenger of superoxide and hydroxyl radicals. 31,32 Furthermore, Robak and Gryglewski 33 have shown that rutin is a scavenger of the superoxide dismutase-sensitive free radicals. It has been reported that flavonoids inhibit xanthine-oxidase, cytochrome P450-dependent estrogen synthase, lipoxygenase and some other enzymes.…”

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confidence: 99%

“…Although flavonoids, which are widely distributed in the plant kingdom, have been recognized to show various biological activities, the effects of specific iNOS inhibition of rutin have not been discussed extensively. 31,33,34 Thus, we designed the present study to determine whether rutin can inhibit iNOS activity and reduce 3-NT formation in the kidneys of rats during I/R. We examined plasma nitrite/nitrate and cGMP concentrations in all experimental groups.…”

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confidence: 99%

Inhibiting inducible nitric oxide synthase with rutin reduces renal ischemia/reperfusion injury

Korkmaz

Kolankaya

2013

Can J Surg

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Background: Nitric oxide (NO) seems to play an important role during renal ischemia/reperfusion (I/R) injury. We investigated whether rutin inhibits inducible nitric oxide synthase (iNOS) and reduces 3-nitrotyrosine (3-NT) formation in the kidneys of rats during I/R. Methods:Wistar albino rats were nephrectomized unilaterally and, 2 weeks later, subjected to 45 minutes of left renal pedicle occlusion followed by 3 hours of reperfusion. We intraperitoneally administered L-N6-(1-iminoethyl)lysine (L-NIL; 3 mg/kg) for 30 minutes or rutin (1 g/kg) for 60 minutes before I/R. After reperfusion, kidney samples were taken for immunohistochemical analysis of iNOS and 3-NT. We measured plasma nitrite/nitrate and cyclic guanosine monophosphate (cGMP) to evaluate NO levels.Results: Ischemia/reperfusion caused plasma cGMP to increase significantly. Similarly, plasma nitrite/nitrate was elevated in the I/R group compared with the control group. Histochemical staining was positive for iNOS and 3-NT in the I/R group. Pretreatment with L-NIL or rutin significantly mitigated the elevation of plasma cGMP and nitrite/nitrate. These changes in biochemical parameters were also associated with changes in immunohistochemical appearance. Pretreatment with L-NIL or rutin significantly decreased the incidence and severity of iNOS and 3-NT formation in the kidney tissues. Conclusion:Our findings suggest that high activity of iNOS causes renal I/R injury, and that rutin exerts protective effects, probably by inhibiting iNOS.Contexte : L'oxyde nitrique (NO) semble jouer un rôle important durant la lésion d'ischémie/reperfusion (I/R) rénale. Nous avons vérifié si la rutine inhibe l'oxyde nitrique synthase inductible (iNOS) et réduit la formation de 3-nitrotyrosine (3-NT) dans les reins de rats durant l'I/R. Méthodes :Des rats albinos Wistar ont subi une néphrectomie unilatérale avant d'être soumis 2 semaines plus tard à une occlusion du pédicule rénal gauche d'une durée de 45 minutes, suivie de 3 heures de reperfusion. Nous avons administré de la L-N6-(1-iminoéthyl)lysine (L-NIL; 3 mg/kg) par voie intrapéritonéale pendant 30 minutes ou de la rutine (1 g/kg) pendant 60 minutes avant l'I/R. Après la reperfusion, des échantillons de tissu rénal ont été prélevés pour analyse immunohistochi mique de l'iNOS et de la 3-NT. Nous avons mesuré les taux plasmatiques de nitrite/nitrate et de guanosine monophosphate cyclique (cGMP) pour évaluer les taux de NO.

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“…This result was supported in the presented study where the GSH level and the GPx, CAT and SOD activities of the lung tissue in the OA group were significantly lower compared to those in the control and rutin 150 mg groups. It is indicated that rutin is an antilipoperoxidant agent [35] and a strong free radical scavenging [36] . Rutin has been indicated to increase the levels of SOD and CAT in rats with cerebral ischemia-reperfusion [37] .…”

Section: Discussionmentioning

confidence: 99%

Ratlarda Oleik Asit Kaynaklı Akut Akciğer Hasarı Üzerine Rutinin Koruyucu Etkileri

Aktaş¹,

Kandemir²,

Özkaraca³

et al. 2017

Kafkas Univ Vet Fak Derg

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Citation of This ArticleAktaş MS, Kandemir FM, Özkaraca M, Hanedan B, Kırbaş A: Protective effects of rutin on acute lung injury induced by oleic acid in rats. Kafkas Univ Vet Fak Derg, 23 (3): 445-451, 2017445-451, . DOI: 10.9775/kvfd.2016 AbstractThe purpose of this study was to explore the protective effects of different doses of rutin with the antioxidant and anti-inflammatory properties on acute lung injury (ALI) induced by oleic acid (OA) in rats. Thirty-five Sprague-Dawley male rats were randomly separated into five groups comprising control, rutin 150 mg, OA, rutin 75 mg + OA and rutin 150 mg + OA. In the rutin 75 mg + OA and rutin 150 mg + OA groups, the lung malondialdehyde level (MDA) was significantly lower than that of the OA group. In the rutin 75 mg + OA and and rutin 150 mg + OA groups, the lung GPx (glutathione peroxidase), CAT (catalase) and SOD (superoxide dismutase) activities and GSH (glutathione) levels were significantly higher than those of the OA group, and significantly lower than those of the control group. iNOS expressions in the interstitial parts of the lungs were significantly lower than those of the OA group. The iNOS expression was lower in the 150 mg + OA group compared to the rutin 75 mg + OA group. It was concluded that on the ALI induced by OA, rutin had protective effects through the antioxidant and antiinflammatory properties and that the treatment of rutin as a supportive treatment in ALI was found to be practically useful. Keywords: Acute lung injury, Oleic acid, Oxidative stress, Rutin Ratlarda Oleik Asit Kaynaklı Akut Akciğer Hasarı Üzerine Rutinin Koruyucu Etkileri ÖzetBu çalışmanın amacı ratlarda rutinin farklı dozlarının antioksidan ve anti-inflamatuar özellikleri yoluyla oleik asit (OA) ile oluşturulan akut akciğer hasarı (ALI) üzerine koruyucu etkilerini araştırmaktı. 35 adet Sprague-Dawley erkek rat kontrol, rutin 150 mg, OA, rutin 75 mg + OA ve rutin 150 mg + OA olmak üzere rasgele 5 gruba ayrıldı. Rutin 75 mg + OA ve rutin 150 mg + OA gruplarında akciğer malondialdehit (MDA) düzeyi OA grubununkine göre önemli düzeyde düşüktü. Rutin 75 mg + OA ve rutin 150 mg + OA gruplarında akciğer GPx (glutasyon peroksidaz), CAT (katalaz), SOD (süperoksit dismutaz) aktiviteleri ile GSH (glutatyon) düzeyleri OA grubununkilere göre önemli düzeyde yüksekti ve kontrol grubununkilere göre önemli düzeyde düşüktü. Rutin 75 mg + OA ve rutin 150 mg + OA gruplarında akciğerlerin interstisyel kısımlarında iNOS ekspresyonları OA grubunkilere göre önemli düzeyde düşüktü. OA ile oluşturulan ALI'de rutinin antioksidan ve antiinflamatuvar özellikler aracılığıyla koruyucu etkilere sahip olduğu, ALI'de destekleyici tedavi amacıyla rutin uygulamasının pratik olarak yararlı olduğu tespit edildi.

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Additional Antilipoperoxidant Activities of Alpha-Tocopherol and Ascorbic Acid on Membrane-Like Systems Are Potentiated by Rutin

Cited by 70 publications

References 19 publications

Alpha-tocopherol inhibits agonist-induced monocytic cell adhesion to cultured human endothelial cells.

Alpha-tocopherol inhibits agonist-induced monocytic cell adhesion to cultured human endothelial cells.

Inhibiting inducible nitric oxide synthase with rutin reduces renal ischemia/reperfusion injury

Ratlarda Oleik Asit Kaynaklı Akut Akciğer Hasarı Üzerine Rutinin Koruyucu Etkileri

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