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

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 μg L−1). Flow cytometry was used to estimate endothelial ICAM‐1 expression. IL‐1β 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 μg L−1) compared to control (mean channel flouresence 81.35 (7.5) vs. 112.5 (9.5), P = 0.01). Supernatant IL‐1β 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.