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Fig. 4 | Journal of Neuroinflammation

Fig. 4

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

Fig. 4

qPCR analysis of enzymes of the kynurenine pathway in brains of TBI victims demonstrates enhanced IDO1 and KYNase expression. Gene expression of six enzymes of the kynurenine pathway was determined by qPCR in four groups of post-mortem brains obtained from the temporal cortex after TBI and uninjured control individuals (n = 10). Groups comprise the following: TBI patients with acute death (survived <17 min after injury, n = 9), TBI patients with delayed death (survival between 6 and 122 h, n = 7) with tissue collected from brain regions having evident tissue pathology (Delay Death Injured Tissue) and brain regions without macroscopic damage obtained from the contralateral uninjured side (Delay Death Normal Tissue) (n = 7). a Indoleamine-pyrrole 2,3-dioxygenase (IDO1), b. kynurenase (KYNase), c kynurenine amino transferase-II (KAT-II), d kynurenine 3-monooxygenase (KMO), e 3-hydroxyanthranilic acid oxygenase (3HAO) and f quinolinic acid phosphoribosyl transferase (QPRTase). Asterisks indicate significant differences (p < 0.05) between TBI and control groups using one-way ANOVA followed by Dunnett’s multiple comparison as post hoc. Data shown as median with 25–75 percentile. IDO1 and KYNase were significantly increased in the Delay Death Injured Tissue group as to the control samples

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