EFFECT OF sCR-1 ON BRAIN POLYMORPHONUCLEAR LEUKOCYTE ACCUMULATION AFTER BRAIN INJURY IN RATS

Kaczorowski, Susan L.; Schiding, Joanne K.; Kochanek, Patrick M.

doi:10.1097/00003246-199401000-00427

Cited by 2 publications

(1 citation statement)

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“…Research concerning the possibly beneficial effects of cytokine blockade or anti‐inflammatory compounds has only recently been initiated. A soluble human recombinant complement (sCR‐1) receptor BRL‐55730 has recently been developed and used with success to inhibit PMNL accumulation and improve neurobehavioural recovery following CCI injury in the rat [ 72]. Post‐traumatic intracerebroventricular (ICV) administration of IL‐1 receptor antagonist (IL‐1ra), which competitively binds to the IL‐1 receptor and inhibits its physiological function, has been shown to reduce the extent of neuronal death (lesion volume) following lateral FP brain injury in the rat [ 201], while systemic administration can improve both cognitive and neurobehavioural motor function and attenuate cell loss in several vulnerable regions including CA3 of the hippocampus, dentate hilar neurons, cortex, and reticular thalamus [ 155].…”

Section: Inflammation and Cytokines: Is Head Injury An Inflammatory Dmentioning

confidence: 99%

gThe Dorothy Russell Memorial Lecture* The molecular and cellular sequelae of experimental traumatic brain injury: pathogenetic mechanisms

McIntosh¹,

Saatman²,

Raghupathi³

et al. 1998

Neuropathology Appl Neurobio

231

108

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The mechanisms underlying secondary or delayed cell death following traumatic brain injury (TBI) are poorly understood. Recent evidence from experimental models of TBI suggest that diffuse and widespread neuronal damage and loss is progressive and prolonged for months to years after the initial insult in selectively vulnerable regions of the cortex, hippocampus, thalamus, striatum, and subcortical nuclei. The development of new neuropathological and molecular techniques has generated new insights into the cellular and molecular sequelae of brain trauma. This paper will review the literature suggesting that alterations in intracellular calcium with resulting changes in gene expression, activation of reactive oxygen species (ROS), activation of intracellular proteases (calpains), expression of neurotrophic factors, and activation of cell death genes (apoptosis) may play a role in mediating delayed cell death after trauma. Recent data suggesting that TBI should be considered as both an inflammatory and/or a neurodegenerative disease is also presented. Further research concerning the complex molecular and neuropathological cascades following brain trauma should be conducted, as novel therapeutic strategies continue to be developed.

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Section: Inflammation and Cytokines: Is Head Injury An Inflammatory Dmentioning

confidence: 99%