Effect of midazolam on in vitro cerebral endothelial ICAM-1 expression induced by astrocyte-conditioned medium.

Abstract:

BACKGROUND AND OBJECTIVE:Astrocytes exposed to hypoxia produce pro-inflammatory cytokines and upregulate intercellular adhesion molecule-1 on cerebral endothelium. This study investigated the effects of midazolam on this response. METHODS:Mouse astrocytes were exposed to 4 h of hypoxia and 24 h of reoxygenation. Astrocyte-conditioned medium were applied to mouse cerebral endothelial cell cultures for 4 h and 24 h in normoxia. Endothelial cells were pre-incubated for 1 h with midazolam (0, 5, 50 microg L-1). Flow cytometry was used to estimate endothelial ICAM-1 expression. IL-1beta concentrations were measured with ELISA. Repeated comparisons were made using ANOVA and post hoc Tukey Test as appropriate. Data are mean (SD). RESULTS:Mouse cerebral endothelial cell ICAM-1 expression was greater after 24 h exposure to hypoxia-reoxygenation astrocyte-conditioned medium compared to normoxic astrocyte-conditioned medium (mean channel flouresence 112.5 (9.5) vs. 81.5 (7.5), P = 0.01). ICAM-1 expression was decreased by midazolam (5 microg L(-1)) compared to control (mean channel flouresence 81.35 (7.5) vs. 112.5 (9.5), P = 0.01). Supernatant IL-1beta concentrations (pg mL(1)) in astrocytes exposed to hypoxia-reoxygenation were greater than those exposed to normoxia (16.41 (2.35) vs. 10.5 (2.13), P = 0.01). CONCLUSION:We conclude that decreased cerebral endothelial ICAM-1 expression in response to activated glial cell compartment by midazolam may decrease post ischaemic brain inflammation and secondary brain injury.

journal_name

Eur J Anaesthesiol

authors

Ghori K,Harmon D,Walsh F,Shorten G

doi

10.1017/S0265021506000652

subject

Has Abstract

pub_date

2006-09-01 00:00:00

pages

788-92

issue

9

eissn

0265-0215

issn

1365-2346

pii

S0265021506000652

journal_volume

23

pub_type

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