Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/73399
Citations | ||
Scopus | Web of Science® | Altmetric |
---|---|---|
?
|
?
|
Type: | Journal article |
Title: | Targeting classical but not neurogenic inflammation reduces peritumoral oedema in secondary brain tumours |
Author: | Lewis, K. Harford-Wright, E. Vink, R. Ghabriel, M. |
Citation: | Journal of Neuroimmunology, 2012; 250(1-2):59-65 |
Publisher: | Elsevier Science BV |
Issue Date: | 2012 |
ISSN: | 0165-5728 1872-8421 |
Statement of Responsibility: | Kate M. Lewis, Elizabeth Harford-Wright, Robert Vink and Mounir N. Ghabriel |
Abstract: | Dexamethasone, the standard treatment for peritumoral brain oedema, inhibits classical inflammation. Neurogenic inflammation, which acts via substance P (SP), has been implicated in vasogenic oedema in animal models of CNS injury. SP is elevated within and outside CNS tumours. This study investigated the efficacy of NK1 receptor antagonists, which block SP, compared with dexamethasone treatment, in a rat model of tumorigenesis. Dexamethasone reverted normal brain water content and reduced Evans blue and albumin extravasation, while NK1 antagonists did not ameliorate oedema formation. We conclude that classical inflammation rather than neurogenic inflammation drives peritumoral oedema in this brain tumour model. |
Keywords: | Blood-Brain Barrier Animals Rats Rats, Wistar Brain Neoplasms Brain Edema Disease Models, Animal Inflammation Dexamethasone Substance P Anti-Inflammatory Agents Male Neurokinin-1 Receptor Antagonists |
Rights: | © 2012 Elsevier B.V. All rights reserved. |
DOI: | 10.1016/j.jneuroim.2012.06.001 |
Published version: | http://dx.doi.org/10.1016/j.jneuroim.2012.06.001 |
Appears in Collections: | Aurora harvest Medical Sciences publications |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.