Figure 4: Effects of a zinc chelator on the ischaemia-induced expression of pro-inflammatory cytokines in the hippocampus.
From: Influence of extracellular zinc on M1 microglial activation

(a–c) Mice were subjected to transient forebrain ischaemia 5 min after intraventricular injection of a zinc chelator, CaEDTA (300 mM in 2 μL volume). Real-time quantitative polymerase chain reaction was performed using total RNA extracted from the hippocampus of mouse brains 3 days after ischaemia. The amount of mRNA for interleukin-1 beta (IL-1β (a), interleukin-6 (IL-6) (b), and tumour necrosis factor-alpha (TNFα (c) was normalised to the amount of mRNA for β-actin. Data are expressed as the mean ± the standard error of the mean (n = 6). *p < 0.05, **p < 0.01, ***p < 0.001, significantly different from the vehicle-treated sham group; #p < 0.05, ##p < 0.01, ###p < 0.005, significantly different from the vehicle-treated ischaemic group. (d–f) Mice were subjected to transient forebrain ischaemia 5 min after intraventricular injection of a non-zinc chelator, ZnEDTA (300 mM in 2 μL volume). Real-time quantitative polymerase chain reaction was performed using total RNA extracted from the hippocampus of mouse brains 3 days after ischaemia. The amount of mRNA for IL-1β (d), IL-6 (e), and was normalised to the amount of (f) was normalised to the amount of mRNA for β-actin. Data are expressed as the mean ± the standard error of the mean (n = 4). *p < 0.05, **p < 0.005, significantly different from the vehicle-treated sham group; #p < 0.01, significantly different from the vehicle-treated ischaemic group.