Comparison of in vitro effects of triflusal and acetysalicylic acid on nitric oxide synthesis by human neutrophils

Miguel, Lourdes Sánchez de; Casado, Santos; Farré, Jerónimo; Garcı́a-Durán, Margarita; Rico, Luís; Montón, Mercedes; Romero, José R.; Bellver, Teresa; Sierra, María P.; Guerra, José; Mata, Pedro; Esteban, Andrés; López‐Farré, Antonio

doi:10.1016/s0014-2999(97)01518-5

Cited by 24 publications

(16 citation statements)

References 29 publications

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“…Moreover, lead-induced up-expression of COX-2 protein was associated with the downregulation of sGC-␤ 1 subunit expression because rofecoxib, an inhibitor of COX-2 activity, attenuated the reduction of sGC-␤ 1 subunit expression. This was further supported by the fact that an inhibitor of protein kinase A activity, H-89 (17), also attenuated the down-expression of sGC-␤ 1 subunit to a similar level as rofecoxib.…”

Section: Discussionmentioning

confidence: 80%

Lead-Induced Downregulation of Soluble Guanylate Cyclase in Isolated Rat Aortic Segments Mediated by Reactive Oxygen Species and Cyclooxygenase-2

Courtois

Marqués²,

Barrientos³

et al. 2003

Journal of the American Society of Nephrology

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Abstract. Lead exposure is a known cause of hypertension. Although most studies have focused on lead-induced endothelial dysfunction and on the involvement of reactive oxygen species (ROS), it has been recently demonstrated that the vascular wall of lead-exposed rats has both an altered the endothelium-independent relaxing response and a reduced expression of soluble guanylate cyclase (sGC). The aim of the present study was to determine in in vitro incubated rat isolated aortic segments if lead downregulates sGC expression, analyzing the involvement of ROS and cyclooxygenase-2 (COX-2). The experiments were performed in isolated aortic segments from Wistar rats that were incubated with lead for 24 h. Lead significantly reduced sGC-␤ 1 subunit expression in a concentration-dependent manner. The maximal reduction in sGC-␤ 1 subunit expression was achieved with 1 ppm lead. Vitamin C (30 mol/L) partially restored sGC-␤1 subunit expression in lead (1 ppm)-exposed aortic segments. A similar protection of sGC-␤ 1 subunit expression was obtained with both a protein kinase A inhibitor, H89 (1 mol/L) and with rofecoxib (1 mol/L), an inhibitor of COX-2 activity. Moreover, lead exposure increased COX-2 expression in the arterial wall. While vitamin C reduced both COX-2 expression and superoxide anion production related to lead exposure, rofecoxib failed to modify superoxide anion generation in lead-incubated aortic segments. In conclusion, the present results suggest the involvement of ROS and COX-2 in the downexpression of sGC-␤ 1 subunit induced by lead in the rat vascular wall.

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Section: Discussionmentioning

confidence: 80%

Lead-Induced Downregulation of Soluble Guanylate Cyclase in Isolated Rat Aortic Segments Mediated by Reactive Oxygen Species and Cyclooxygenase-2

Courtois

Marqués²,

Barrientos³

et al. 2003

Journal of the American Society of Nephrology

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“…10) After triflusal treatment, the neutrophils demonstrated a higher ability to prevent ADP-induced platelet aggregation. 9) The antithrombotic properties of triflusal in inhibiting thromboxane synthesis and in increasing cAMP and nitric oxide contributed greatly to the prevention of serious vascular events in people at high risk.…”

Section: Discussionmentioning

confidence: 99%

“…8) Triflusal and HTB have been reported to have anti-inflammatory and vasodilatory effects in addition to the antiplatelet effect. [9][10][11] Triflusal reduces serious vascular events, especially in high risk patients with a previous history of ischemic strokes, myocardial infarction, or peripheral artery disease.…”

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confidence: 99%

Comparison of Triple Antiplatelet Therapy Including Triflusal and Conventional Dual Therapy in Patients Who Underwent Drug-Eluting Stent Implantation

et al. 2009

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SummaryTriflusal is a derivative of acetylsalicylic acid but it exhibits different pharmacological and pharmacokinetic properties. The object of this study was to evaluate the efficacy of additional use of triflusal in patients who underwent drug-eluting stent implantation.First, we prospectively tested platelet function with a rapid platelet function analyzer (VerifyNow Ⓡ -Aspirin) in patients with stable angina (male, age, 61.6 ± 8.3, body weight, 69.3 ± 11.2 kg) who maintained dual (aspirin 100 mg and clopidogrel 75 mg per day, n = 23) or triple (aspirin 100 mg, clopidogrel 75 mg, and triflusal 300 mg per day, n = 23) therapy for more than one month. They were randomly assigned to a group. The triple group showed superior inhibition of arachidonic acid induced platelet aggregation compared to the dual group (420.2 ± 47.7 ARU versus 465.0 ± 71.2 ARU, P = 0.016). Second, we compared composite outcomes (death, myocardial infarction, and nonhemorrhagic stroke) after drug-eluting stent (DES) implantation between the dual (n = 1474) and triple (n = 433) groups in the prospective Seoul National University Hospital drug-eluting stent (SNUH-DES) cohort. The triple group had more current smokers, male patients, and patients with a previous history of revascularization. Also, the triple group underwent more complex interventions such as left main, chronic total occlusion, long lesion, and restenotic lesion than the dual group. In spite of their higher risk profiles, the triple group patients showed comparable composite outcomes (19 cases, 4.4%) to those of the dual group ones (41 cases, 2.8%) (P = 0.12). The triflusal-based triple antiplatelet therapy achieved superior platelet inhibition compared to the dual therapy ex vivo and it could be applied after complex intervention with DES. (Int Heart J 2009; 50: 701-709)

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“…By virtue of COX-1 inhibition, triflusal also inhibits thromboxane biosynthesis (23, 24 -28). Furthermore, triflusal leads to increased cAMP levels in platelets by inhibition of cAMP-phosphodiesterase activity (29), is associated with protection of prostacyclin biosynthesis due to its negligible inhibitory effect on vascular cyclooxygenase at therapeutic doses (23, 26 -28), and stimu- lates nitric oxide release by human neutrophiles (30,31). Even though triflusal is less potent than salicylic acid as COX-1 inhibitor (15,(22)(23)(24), triflusal and its main metabolite HTB are more potent than aspirin in inhibiting the activation of NF-B (32), and inhibition of this transduction factor may be related with an improvement of insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

Salicylates Increase Insulin Secretion in Healthy Obese Subjects

Fernández-Real

López‐Bermejo

Ropero

et al. 2008

The Journal of Clinical Endocrinology &Amp; Metabolism

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Comparison of in vitro effects of triflusal and acetysalicylic acid on nitric oxide synthesis by human neutrophils

Cited by 24 publications

References 29 publications

Lead-Induced Downregulation of Soluble Guanylate Cyclase in Isolated Rat Aortic Segments Mediated by Reactive Oxygen Species and Cyclooxygenase-2

Lead-Induced Downregulation of Soluble Guanylate Cyclase in Isolated Rat Aortic Segments Mediated by Reactive Oxygen Species and Cyclooxygenase-2

Comparison of Triple Antiplatelet Therapy Including Triflusal and Conventional Dual Therapy in Patients Who Underwent Drug-Eluting Stent Implantation

Salicylates Increase Insulin Secretion in Healthy Obese Subjects

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