Blood-Brain Barrier Permeability, Neutrophil Accumulation and Vascular Adhesion Molecule Expression after Controlled Cortical Impact in Rats: A Preliminary Study

Whalen, Michael J.; Carlos, Timothy M.; Kochanek, Patrick M.; Heineman, Scott

doi:10.1007/978-3-7091-6475-4_61

Cited by 30 publications

(29 citation statements)

References 6 publications

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“…The expression of E-and P-selectins on cerebral blood vessels has been described previously in models of permanent or transient middle cerebral artery occlusion in rats and in animal models of head trauma (Whalen et al, 1998).…”

Section: Expression Of E-selectins and P-selectins On Adult And Juvenmentioning

confidence: 73%

Recruitment of Neutrophils across the Blood–Brain Barrier: The Role of E- and P-selectins

Bernardes-Silva

Anthony²,

Issekutz

et al. 2001

J Cereb Blood Flow Metab

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Summary:The adult central nervous system parenchyma is resistant to inflammation, but in juvenile rats the injection of inflammatory mediators, interleukin-1␤ for example, gives rise to extensive neutrophil recruitment and neutrophil-dependent blood-brain barrier breakdown. The factors that confer this resistant phenotype are unknown. In this study, the authors demonstrate that E-and P-selectin expression is increased to a similar extent in adult and juvenile brain after the intracerebral injection of IL-1␤. Thus, the refractory nature of the brain parenchyma cannot be attributed to an absence of selectin expression. However, in injuries where the resistant characteristic of the brain parenchyma is compromised, and neutrophil recruitment occurs, selectin blockade may be an advantage. The authors investigated the contribution that selectins make to neutrophil recruitment during acute inflammation in the brain. The authors examined neutrophil recruitment by immunohistochemistry on brain sections of juvenile rats killed four hours after the intracerebral injection of IL-1␤ and the intravenous injection of neutralizing anti-selectin monoclonal antibodies (mAb). The administration of the P-selectin blocking mAb inhibited neutrophil recruitment by 85% compared with controls. Surprisingly, E-selectin blockade had no effect on neutrophil recruitment to the brain parenchyma. Thus, P-selectin appears to play a pivotal role in mediating neutrophil recruitment to the brain parenchyma during acute inflammation.

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Section: Expression Of E-selectins and P-selectins On Adult And Juvenmentioning

confidence: 73%

Recruitment of Neutrophils across the Blood–Brain Barrier: The Role of E- and P-selectins

Bernardes-Silva

Anthony²,

Issekutz

et al. 2001

J Cereb Blood Flow Metab

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“…Several studies have shown that CCI injury causes an increase in vascular permeability (Baldwin et al, 1996;Baskaya et al, 1997;DeWitt and Prough, 2003;Whalen et al, 1998). Based on the preservation of claudin-5 levels we observed, we questioned if this was associated with improved BBB integrity.…”

Section: Post-injury Cape Administration Reduces Tbi-associated Vascumentioning

confidence: 86%

Caffeic Acid Phenethyl Ester Protects Blood–Brain Barrier Integrity and Reduces Contusion Volume in Rodent Models of Traumatic Brain Injury

Zhao¹,

Pati

Redell³

et al. 2012

Journal of Neurotrauma

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A number of studies have established a deleterious role for inflammatory molecules and reactive oxygen species (ROS) in the pathology of traumatic brain injury (TBI). Caffeic acid phenethyl ester (CAPE) has been shown to exert both antioxidant and anti-inflammatory effects. The primary objective of the present study was to examine if CAPE could be used to reduce some of the pathological consequences of TBI using rodent models. Male Sprague-Dawley rats and C57BL/6 mice were subjected to controlled cortical impact (CCI) injury. Blood -brain barrier (BBB) integrity was assessed by examining claudin-5 expression and the extravasation of Evans blue dye. The effect of post-injury CAPE administration on neurobehavioral function was assessed using vestibulomotor, motor, and two hippocampus-dependent learning and memory tasks. We report that post-TBI administration of CAPE reduces Evans blue extravasation both in rats and mice. This improvement was associated with preservation of the levels of the tight junction protein claudin-5. CAPE treatment did not improve performance in either vestibulomotor/motor function (tested using beam balance and foot-fault tests), or in learning and memory function (tested using the Morris water maze and associative fear memory tasks). However, animals treated with CAPE were found to have significantly less cortical tissue loss than vehicle-treated controls. These findings suggest that CAPE may provide benefit in the treatment of vascular compromise following central nervous system injury.

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“…However, our doses of L-NIL were similar to those used to attenuate systemic nitrite production in rats after endotoxin administration (45). Although the blood-brain barrier (BBB) penetration of L-NIL is uncertain, the BBB is permeable to albumin for at least 8 hours after CCI (74).…”

Section: Figurementioning

confidence: 97%

Inducible nitric oxide synthase is an endogenous neuroprotectant after traumatic brain injury in rats and mice

et al. 1999

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Blood-Brain Barrier Permeability, Neutrophil Accumulation and Vascular Adhesion Molecule Expression after Controlled Cortical Impact in Rats: A Preliminary Study

Cited by 30 publications

References 6 publications

Recruitment of Neutrophils across the Blood–Brain Barrier: The Role of E- and P-selectins

Recruitment of Neutrophils across the Blood–Brain Barrier: The Role of E- and P-selectins

Caffeic Acid Phenethyl Ester Protects Blood–Brain Barrier Integrity and Reduces Contusion Volume in Rodent Models of Traumatic Brain Injury

Inducible nitric oxide synthase is an endogenous neuroprotectant after traumatic brain injury in rats and mice

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