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. 2017 Jan 19;7:41032. doi: 10.1038/srep41032

Table 2. Analysis of the markers of biomolecular pathway of damage induced by bilirubin.

  Hip Cll IC SC Ctx
Ho1 3.97 ± 1.09c 2.55 ± 0.95b 3.39 ± 0.92c 2.51 ± 0.67a 1.65 ± 0.09
Srnx1 14.90 ± 2.79c 4.38 ± 3.15a 17.42 ± 5.65a 9.12 ± 4.83b 1.44 ± 1.12
Tnfα 3.58 ± 2.17a 2.06 ± 1.3 1.81 ± 0.94 2.25 ± 0.32c 1.08 ± 0.61
Il1β 13.69 ± 7.17b 8.83 ± 6.08a 23.96 ± 10.58c 5.38 ± 2.8c 2.89 ± 1.51a
Il6 305.08 ± 120.22c 9.64 ± 5.04c 98.92 ± 38.35c 122.08 ± 126.10a 12.39 ± 7.61c
Cox2 53.64 ± 11.12c 62.19 ± 29.95c 56.08 ± 21.88c 2.48 ± 2.06a 3.53 ± 2.44a
Glu 2.39 ± 0.31c 1.20 ± 0.25 2.03 ± 0.59b 1.23 ± 0.18 1.21 ± 0.18

The expression of selected genes, used as markers of biomolecular pathways of damage induced by bilirubin, was expressed as fold change of the control (DMSO-challenged OBCs). Similarly, quantification of glutamate release in the medium of Bf-challenged OBCs was expressed as the fold change of DMSO-exposed cultures. Ho1: heme oxygenase1; Srnx1: sulfiredoxin 1; Tnfα: tumor necrosis factor alfa; Il1β: interleukin 1β; Cox2: cyclo-oxygenase 2. Data are expressed as the mean ± SD of three-five repetitions. Statistical significance: ap < 0.05; bp < 0.01; cp < 0.001. Hip: hippocampus; Cll: cerebellum; IC: inferior colliculus; SC: superior colliculus; Ctx: cortex.