Effect of COX-2 inhibitor meloxicam against traumatic brain injury-induced biochemical, histopathological changes and blood–brain barrier permeability

Hakan, Tayfun; Toklu, Hale Z.; Biber, Necat; Özevren, Hüseyin; Solakoğlu, Seyhun; Demırtürk, Pelin; Aker, Fügen

doi:10.1179/016164109x12464612122731

Cited by 49 publications

(38 citation statements)

References 35 publications

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“…They showed that the immune reaction peaks between 24-72 hours after injury and the neuroprotective effect of treatment with COX-2 inhibitors begins 6 hours after injury (7). Various researchers have observed increased motor performance after neurotrauma and ischemia with COX-2 inhibitors in animal models (5,8). In our study, animals were sacrificed 24 hours after trauma, which allowed time for the effects of COX-2 inhibition to occur.…”

Section: Discussionmentioning

confidence: 99%

“…In our study, the higher levels of superoxide dismutase activity induced by TBI decreased with lornoxicam treatment. Other COX-2 inhibitors besides lornoxicam have also been reported to have antioxidant effects, in addition to their anti-inflammatory actions (2,8).…”

Section: Discussionmentioning

confidence: 99%

“…Free radicals damage cell contents such as lipids, protein and DNA. Antioxidant and anti-inflammatory drugs have been comprehensively studied in neurotrauma models (8,31). Cyclooxygenase inhibitors act as neuroprotective agents by decreasing the formation of prostanoid and free radicals or by directing arachidonic acid metabolism to different metabolic ways (7,11,34).…”

Section: Discussionmentioning

confidence: 99%

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The effects of lornoxicam on neuroprotection following diffuse traumatic brain injury in rats

Topçu

Vatansever²,

Bayram³

et al. 2013

Turkish Neurosurgery

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AIm:In this study, the effects of lornoxicam on the prevention of secondary brain injury via the apoptotic pathway were studied in a rat model of head injury. mAterIAl and methOds: Thirty adult male Wistar albino rats were anesthetized, and experimental closed head trauma was induced by allowing a 450 g weight to fall two meters onto a metallic disk fixed to the intact skull. After head injury, the rats were randomly divided into two groups: Group I (n=15) rats were administered 2 mL saline intraperitoneally (controls); Group II (n=15) rats were administered 2 mL 1.3 mg kg -1 lornoxicam intraperitoneally. Brain tissue samples were divided into two pieces by interhemispheric incision for biochemical and histological analysis. results: TUNEL positivity was seen in neuroglia cells of the brain cortex in both groups. While the immunoreactivities of caspase 8, 9 and Fas/ Fas ligand were similar in both groups, the immunoreactivity of caspase 3 was greater in Group I than Group II. MDA was significantly lower in Group II than in Group I (p<0.05). The decrease in SOD level was higher in Group I than Group II. COnClusIOn:Lornoxicam did not prevent apoptosis in this rat model of brain trauma but causes a decrease.KeywOrds: Traumatic brain injury, Lornoxicam, Apoptosis, Neuroprotection, Rats ÖZ AmAÇ: Bu çalışmada, lornoksikamın sekonder beyin hasarını önlemede, kafa travmalı bir rat modelinde apoptotik yollar aracılı etkileri araştırıldı. yÖntem ve GereÇler: Otuz erişkin Wistar albino rata anestezi uygulaması sonrası kafatası üzerine konan bir metal disk üzerine 2 metreden 450 g ağırlık düşürülerek deneysel kapalı kafa travması oluşturuldu. Travma sonrası ratlar randomize olarak 2 gruba ayrıldı; Grup I'e (n=15) intraperitoneal yolla 2 mL salin, Grup II (n=15) intraperitoneal yolla 2 mL 1.3 mg kg -1 lornoksikam verildi. Beyin dokuları biyokimyasal ve histolojik incelemeler için interhemisferik kesi ile ikiye ayrıldı.BulGulAr: TUNEL pozitifliği her iki grupta beyin korteks nöroglia hücrelerinde görüldü. Her iki grupta kaspaz 8, 9 ve Fas/Fas ligand immünoreaktivitesi normalken, kaspaz 3 immünoreaktivitesi Grup I'de Grup II'den daha yüksekti. MDA Grup II'de Grup I'den daha düşüktü. SOD düzeyindeki azalma Grup I'de, Grup II'den daha fazlaydı. sOnuÇ: Lornoksikam bu beyin travması rat modelimizde apoptozisi önlememiş ancak bir azalma sağlamıştır.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The effects of lornoxicam on neuroprotection following diffuse traumatic brain injury in rats

Topçu

Vatansever²,

Bayram³

et al. 2013

Turkish Neurosurgery

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“…[11] Meloxicam, a COX-2 inhibitor, has been found to preserve BBB permeability, decrease anti-inflammatory activity, and decrease brain edema in a model of diffuse TBI. [21] The central nervous system inflammatory reaction occurring after aneurysmal subarachnoid hemorrhage and intracerebral hemorrhage involves the upregulation of numerous cytokines and prostaglandins. [22,23] After intracerebral hemorrhage, COX inhibition with celecoxib, a selective COX-2 inhibitor, decreases brain edema, inflammation, and perihematomal cell death by decreasing generation of prostaglandin E2.…”

Section: Discussionmentioning

confidence: 99%

The effects of lornoxicam on brain edema and blood brain barrier following diffuse traumatic brain injury in rats

Topçu

Gümüşer²,

Bayram³

et al. 2013

Ulus Travma Acil Cerrahi Derg

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“…To evaluate the blood-brain barrier integrity, Evans blue (EB) dye was used as a marker of albumin extravasation (22). EB was expressed as μg/mg of brain tissue against a standard curve…”

Section: Evans Blue Assay For Blood˗brain Barrier Permeabilitymentioning

confidence: 99%

Histopathological changes in the choroid plexus after traumatic brain injury in the rats: a histologic and immunohistochemical study

2015

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Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analyzed the histopathological changes in E-cadherin and VEGF expression after traumatic brain injury in rats. The rats were divided into 2 groups as the control and the trauma groups. Sprague-Dawley rats were subjected to traumatic brain injury with a weight-drop device using 300 g -1 m weight-height impact. After 5 days of traumatic brain injury, blood samples were taken under ketamine hydroxide anesthesia and biochemical analyzes were performed. The control and trauma groups were compared in terms of biochemical values. There was no change in glutathione (GSH) levels and blood brain barrier permeability. However, malondialdehyde (MDA) and myeloperoxidase activity (MPO) levels increased in the trauma group. In the histopathological examination, choroid plexus in the lateral ventricule, near the piamater membrane, was removed. In the traumatic group, some of epithelial cells were hyperplasic, some of were with local degeneration with peeled off from apical surface. In addition, we observed that congestion in capillary vessels and mononuclear cell infiltration around the vessels. After traumatic brain injury, the increase in vascular endothelial growth factor (VEGF) levels, vascular permeability, and interaction with VEGF receptors in endothelial cells lead to edema in the vessel wall. On the other hand, E-cadherin expression decreased in the tight-junction structures between epithelial cells and basal membrane, resulting in an increase in cerebrospinal fluid in the intervillous area.

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Effect of COX-2 inhibitor meloxicam against traumatic brain injury-induced biochemical, histopathological changes and blood–brain barrier permeability

Abstract: Meloxicam exerts neuroprotective effect by preserving BBB permeability and by reducing brain edema (probably by its anti-inflammatory properties) in the diffuse brain injury model.

Cited by 49 publications

References 35 publications

The effects of lornoxicam on neuroprotection following diffuse traumatic brain injury in rats

The effects of lornoxicam on neuroprotection following diffuse traumatic brain injury in rats

The effects of lornoxicam on brain edema and blood brain barrier following diffuse traumatic brain injury in rats

Histopathological changes in the choroid plexus after traumatic brain injury in the rats: a histologic and immunohistochemical study

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