Effects of triflusal on oxidative stress, prostaglandin production and nitric oxide pathway in a model of anoxia-reoxygenation in rat brain slices

Correa, José Antonio González; Arrebola, María Monsalud; Ureña, I.; Guerrero, A.; Muñoz‐Marín, J.; Ruiz‐Villafranca, D.; Cuesta, Felipe Sánchez de la; Cruz, J. P. De La

doi:10.1016/j.brainres.2004.02.069

Cited by 10 publications

(9 citation statements)

References 31 publications

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“…aspirin did not significantly affect LDH activity, while triflusal, at the recommended antithrombotic dose of 10 mg/kg/day, inhibited LDH activity by 42%. Similar differences between the two drugs were observed in their effects on the bio-chemical pathways of brain damage (oxidative stress, prostaglandin accumulation and nitric oxide pathway, among others) (33).…”

Section: Neuroprotective Effectsupporting

confidence: 54%

“…By oral administration at 30 mg/kg triflusal reduced brain lesions caused by the intracerebral injection of N-methyl-D-aspartate (NMDA) (1,3). In addition, by chronic oral administration at 1, 10, or 50 mg/kg trifusal significantly reduced brain damage caused by anoxia-reoxygenation of rat brain slices, diminishing the activity of LDH (an indirect indicator of brain cell death in this experimental model) by 21, 42, and 47%, respectively (33). Acetylsalicylic acid had dose-dependent, but quantitatively lesser neuroprotective effect.…”

Section: Neuroprotective Effectmentioning

confidence: 89%

“…Studies of the neuroprotective effect of triflusal and its metabolite HTB consistently showed that the effect of the latter is at least as intense, if not more so, than the effect of triflusal, and that HTB is consistently more effective than its salicylic acid counterpart (1,3,33,34).…”

Section: Neuroprotective Effectmentioning

confidence: 99%

“…A number of recent experimental and clinical studies have shown that triflusal is a potentially useful choice in the treatment and prophylaxis of brain ischemia because of its antithrombogenic as well as neuroprotective effects. Its antithrombogenic properties have been demonstrated clinically and experimentally, while its neuroprotective effects have been shown only in animal models (1)(2)(3)33,34,42). In this article we review the most important features of triflusal, with particular attention to its effect on brain ischemia.…”

Section: Introductionmentioning

confidence: 99%

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Triflusal: An Antiplatelet Drug with a Neuroprotective Effect?

Correa

Cruz

2006

Cardiovascular Drug Reviews

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Triflusal is a derivative of salicylic acid with a well-established platelet aggregation inhibitory profile. Its pharmacokinetic and pharmacodynamic properties differ, however, somewhat from those of acetylsalicylic acid. A number of recent experimental and clinical studies have shown that triflusal is a potentially useful choice in the treatment and prophylaxis of brain ischemia because of its antithrombogenic as well as neuroprotective effects. Its antithrombogenic effect has been demonstrated at the clinical as well as at the experimental level, while its neuroprotective effect has been shown only in experimental models. The drug interferes with thrombogenesis by inhibiting thromboxane synthesis and increasing the levels of cAMP and nitric oxide. Its neuroprotective action is the result of its antioxidant and antiinflammatory effects in brain tissue. From a clinical standpoint triflusal is similar in efficacy to acetylsalicylic acid in preventing stroke, but has less adverse effects, especially it is less likely to cause bleeding. Because of its pharmacodynamic properties and lower rate of adverse reactions, triflusal may be a useful alternative to acetylsalicylic acid in the prevention of stroke.

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Section: Neuroprotective Effectsupporting

confidence: 54%

Section: Neuroprotective Effectmentioning

confidence: 89%

Section: Neuroprotective Effectmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Triflusal: An Antiplatelet Drug with a Neuroprotective Effect?

Correa

Cruz

2006

Cardiovascular Drug Reviews

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“…As a result, hypoxic injury may have drastic effects on brain development (when the stress is in early life) and function. Prolonged brain hypoxia can cause an increase in cerebral blood flow, glucose metabolism and glycolysis, oxidative stress and altered intracellular production of prostaglandins (Harik et al, 1994;Niwa et al, 2000;Leffler CW and Perfenova H, 1997;Gonzalez-Correa et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin transporter expression in mouse brain during development and in response to hypoxia

et al. 2007

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Prostaglandins (PGs) are bioactive lipid mediators released following brain hypoxic-ischemic injury. Clearance and re-uptake of these prostaglandins occur via a transmembrane prostaglandin transporter (PGT), which exchanges PG for lactate. We used western blot analyses to examine the PGT developmental profile and its regional distribution as well as changes in transporter expression during chronic hypoxia. Microsomal preparations from four brain regions (cortex, hippocampus, cerebellum and brainstem/diencephalon) showed gradual increases in prostaglandin transporter expression in all brain regions examined from postnatal day 1 till day 30. There was a significant regional heterogeneity in the prostaglandin transporter expression with highest expression in the cortex, followed by cerebellum and hippocampus, and least expressed in the brainstem-diencephalon. To further delineate the pattern of prostaglandin transporter expression, separate astrocytic and neuronal microsomal preparations were also examined. In contrast to neurons, which had a robust expression of prostaglandin transporters, astrocytes had very little PGT expression under basal conditions. In response to chronic hypoxia, there was a significant decline in PGT expression in vivo and in neurons in vitro, whereas cultured astrocytes increased their PGT expression. This is the first report on PGT expression in the central nervous system (CNS) and our studies suggest that PGTs have 1) a widespread distribution in the CNS; 2) a gradual increase and a differential expression in various regions during brain development; and 3) striking contrast in expression between glia and neurons, especially in response to hypoxia. Since PGTs play a role as prostaglandin-lactate exchangers, we hypothesize that PGTs are important in the CNS during stress such as hypoxia.

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