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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Activation of the kynurenine pathway and increased production of the excitotoxin quinolinic acid following traumatic brain injury in humans

Fig. 5

Immunohistochemistry of post-mortem brains reveals increased IDO1 acutely after TBI. a IDO1 immunohistochemistry was performed on post-mortem brains as described in the ‘Materials and methods’ section. IDO1 is found increasingly expressed in Acute Death and Delayed Death Injured Tissue samples compared to the control. Top panels (i, iii, v, vii) indicate ×200 magnification; bottom panels (ii, iv, vi, viii) indicate ×600 magnification. Figures represent IDO1 immunohistochemistry of the cortex of the uninjured control group (i and ii), acute death (<17 min after injury; Acute Death) (iii and iv), tissue obtained from injured cortex of TBI patients with delayed death (survival between 6 and 122 h; Delay Death Injured Tissue) (v and vi) and tissue collected from regions without macroscopic damage of the contralateral uninjured side (Delay Death Normal Tissue) (vii and viii). Rectangular boxes in the ×200 panels indicate the magnified regions of ×600. Brain sections were counterstained with haematoxylin. b IDO immunohistochemistry staining was semi-quantitatively assessed in post-mortem brain samples and presented as the percentage of positively stained cells relative to the total number of cells per field. Statistical differences were calculated as described in the Materials and methods section, *p ≤ 0.05. Data are mean ± SEM. Significant increase in the number of IDO1-positive cells was observed in Acute Death and Delayed Death Injured Tissue as compared to the controls; similar levels of IDO1-positive cells were between Control and Delayed Death Normal Tissue groups

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