Overexpression of Cyclooxygenase-2 in Rabbit Basilar Artery Endothelial Cells after Subarachnoid Hemorrhage

Yr, Tran Dinh; Jomaa, Ahmad; Crinon, Jacques; Am, Reynier-Rebuffel; Tedgui, Alain; Savarit, A; Sercombe, Richard

doi:10.1097/00006123-200103000-00037

Cited by 33 publications

(10 citation statements)

References 37 publications

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“…We observed that hemolysate induced the production of several inflammatory mediators as well as the activation of NF-кB in vitro . We also confirmed that COX-2 and iNOS were produced in the rat femoral artery model, similar to the results with experimental SAH models previously described [19,20]. Our in vivo and in vitro studies clearly showed trehalose suppressed these inflammatory responses.…”

Section: Discussionsupporting

confidence: 91%

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Trehalose treatment suppresses inflammation, oxidative stress, and vasospasm induced by experimental subarachnoid hemorrhage

et al. 2012

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BackgroundSubarachnoid hemorrhage (SAH) frequently results in several complications, including cerebral vasospasm, associated with high mortality. Although cerebral vasospasm is a major cause of brain damages after SAH, other factors such as inflammatory responses and oxidative stress also contribute to high mortality after SAH. Trehalose is a non-reducing disaccharide in which two glucose units are linked by α,α-1,1-glycosidic bond, and has been shown to induce tolerance to a variety of stressors in numerous organisms. In the present study, we investigated the effect of trehalose on cerebral vasospasm, inflammatory responses, and oxidative stress induced by blood in vitro and in vivo.MethodsEnzyme immunoassay for eicosanoids, pro-inflammatory cytokines, and endothelin-1, and western blotting analysis for cyclooxygenase-2, inducible nitric oxide synthase, and inhibitor of NF-κB were examined in macrophage-like cells treated with hemolysate. After treatment with hemolysate and hydrogen peroxide, the levels of lipid peroxide and amounts of arachidonic acid release were also analyzed. Three hours after the onset of experimental SAH, 18 Japanese White rabbits received an injection of saline, trehalose, or maltose into the cisterna magna. Angiographic and histological analyses of the basilar arteries were performed. In a separate study, the femoral arteries from 60 rats were exposed to fresh autologous blood. At 1, 3, 5, 7, 10, and 20 days after treatment, cryosections prepared from the femoral arteries were histologically analyzed.ResultsWhen cells were treated with hemolysate, trehalose inhibited the production of several inflammatory mediators and degradation of the inhibitor of NF-κB and also suppressed the lipid peroxidation, the reactive oxygen species-induced arachidonic acid release in vitro. In the rabbit model, trehalose produced an inhibitory effect on vasospasm after the onset of experimental SAH, while maltose had only a moderate effect. When the rat femoral arteries exposed to blood were investigated for 20 days, histological analysis revealed that trehalose suppressed vasospasm, inflammatory response, and lipid peroxidation.ConclusionsThese data suggest that trehalose has suppressive effects on several pathological events after SAH, including vasospasm, inflammatory responses, and lipid peroxidation. Trehalose may be a new therapeutic approach for treatment of complications after SAH.

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Section: Discussionsupporting

confidence: 91%

“…These cells play important roles in inflammation after SAH [19-22]. The hemolysate (see below) was used for in vitro studies on blood-induced inflammation.…”

Section: Methodsmentioning

confidence: 99%

Trehalose treatment suppresses inflammation, oxidative stress, and vasospasm induced by experimental subarachnoid hemorrhage

et al. 2012

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“…Recent studies have shown that many of the inflammation‐related genes are upregulated in vasospastic arteries relative to control 24 . Upregulation of cyclo‐oxygenase‐2 25 and 5‐LOX 18 in rabbit and canine basilar artery after SAH has also been reported. Furthermore, it was found that the 5‐LOX inhibitors are effective in preventing or attenuating cerebral vasospasm in rabbit and canine models of SAH 26,27 .…”

Section: Discussionmentioning

confidence: 92%

Participation of Vasopressin in the Development of Cerebral Vasospasm in a Rat Model of Subarachnoid Haemorrhage

Trandafir

Nishihashi

Wang

et al. 2004

Clin Exp Pharma Physio

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1. Previous studies have suggested the involvement of arginine vasopressin (AVP) and inflammation in the development of cerebral vasospasm after subarachnoid haemorrhage (SAH). The aim of the present study was to clarify the role of AVP in the arterial narrowing following cerebral haemorrhage by examining the effect of SR 49059 (a V(1) receptor antagonist) on the diameter of rat basilar artery exposed to SAH. The effect of the 5-lipoxygenase inhibitor ZM 230487 on AVP-induced contraction of rat basilar arteries was also investigated. 2. After 1 h and 2 days from SAH induction, brains were removed and pictures of the basilar arteries were taken. The external diameter of the basilar artery was measured in the presence and absence of SR 49059 (1 mg/kg, i.v.). For in vitro experiments, the basilar arteries isolated from control and SAH rats (at 1 h and at 2 days from SAH induction) were cut into spiral preparations and the AVP (0.3 nmol/L)-induced contraction in the presence of ZM 230487 was investigated. Each group analysed (i.e. control, SAH 1 h and SAH 2 days) consisted of eight rats. 3. The diameter of rat basilar arteries decreased by 43 and 25% at 1 h and 2 days from SAH induction, respectively, compared with control. The administration of SR 49059 significantly reduced cerebral vasospasm. After SAH induction, the diameter of the basilar artery in SR 49059-treated groups decreased by only 22% (at 1 h) and by 3% (at 2 days) compared with the control group (P < 0.01). In basilar arterial strips, ZM 230487 attenuated the vasopressin-induced contraction in both control and SAH groups. However, SAH groups showed a significant resistance of the AVP-induced contraction in the presence of ZM 230487 compared with control (P < 0.05). 4. The results suggest that the cerebral vasospasm in SAH rats is due, at least in part, to endogenous AVP and may involve an increase in the activity of 5-lipoxygenase. SR 49059 may represent a potential therapeutic strategy for the treatment of cerebral vasospasm.

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“…41, 44 Celecoxib is likely to provide neuroprotective and anti-inflammatory effects via to its clinically utilized COX-2 inhibitory activity. 45-47 …”

Section: Discussionmentioning

confidence: 99%

Vascular KCNQ (Kv7) Potassium Channels as Common Signaling Intermediates and Therapeutic Targets in Cerebral Vasospasm

Mani

O'Dowd

Kumar

et al. 2013

Journal of Cardiovascular Pharmacology

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Cerebral vasospasm following subarachnoid hemorrhage (SAH) is characterized by prolonged severe constriction of the basilar artery, which often leads to ischemic brain damage. Locally elevated concentrations of spasmogenic substances induce persistent depolarization of myocytes in the basilar artery, leading to continuous influx of calcium (Ca2+) through voltage-sensitive Ca2+ channels and myocyte contraction. Potassium (K+) channel openers may have therapeutic utility to oppose membrane depolarization, dilate the arteries, and reduce ischemia. Here, we examined the involvement of vascular Kv7 K+ channels in the pathogenesis of cerebral vasospasm and tested whether Kv7 channel openers are effective therapeutic agents in a rat model of SAH. Patch-clamp experiments revealed that three different spasmogens (serotonin, endothelin and vasopressin) suppressed Kv7 currents and depolarized freshly isolated rat basilar artery myocytes. These effects were significantly reduced in the presence of a Kv7 channel opener, retigabine. Retigabine (10 μmol/L) also significantly blocked L-type Ca2+ channels, reducing peak inward currents by >50%. In the presence of a selective Kv7 channel blocker, XE991, the spasmogens did not produce additive constriction responses measured using pressure myography. Kv7 channel openers (retigabine or celecoxib) significantly attenuated basilar artery spasm in rats with experimentally-induced SAH. In conclusion, we identify Kv7 channels as common targets of vasoconstrictor spasmogens and as candidates for therapeutic intervention for cerebral vasospasm.

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Overexpression of Cyclooxygenase-2 in Rabbit Basilar Artery Endothelial Cells after Subarachnoid Hemorrhage

Cited by 33 publications

References 37 publications

Trehalose treatment suppresses inflammation, oxidative stress, and vasospasm induced by experimental subarachnoid hemorrhage

Trehalose treatment suppresses inflammation, oxidative stress, and vasospasm induced by experimental subarachnoid hemorrhage

Participation of Vasopressin in the Development of Cerebral Vasospasm in a Rat Model of Subarachnoid Haemorrhage

Vascular KCNQ (Kv7) Potassium Channels as Common Signaling Intermediates and Therapeutic Targets in Cerebral Vasospasm

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