Skip to main content
Figure 4 | Journal of Neuroinflammation

Figure 4

From: Indomethacin protects rats from neuronal damage induced by traumatic brain injury and suppresses hippocampal IL-1β release through the inhibition of Nogo-A expression

Figure 4

Effects of TBI, Nogo-A irrelevant control oligonucleotide, Nogo-A antisense oligonucleotide, and indomethacin administration on the production of IL-1β. All samples were obtained eight hours after TBI. The relative level of the released IL-1β is compared among different treatment groups: neither TBI nor drug (sham); TBI and Nogo-A irrelevant control oligonucleotide (TBI + Irr), TBI and Nogo-A antisense oligonucleotide (TBI + Nogo-A antisense); TBI and solvent vehicle (75% alcohol) (TBI + vehicle); and TBI combined with indomethacin injection (TBI + indomethacin). (A) RT-PCR analysis of the expression of IL-1β among different groups along with the analysis of actin transcription as an internal control. (B) Quantification of IL-1β expression. (C) ELISA analysis on the expression of IL-1β protein levels among different groups. Bars represent the means ± SEM values (n = 5). *P <0.05 is considered significantly different from the sham value using the Mann–Whitney U test, and #P <0.05 is considered significantly different from the TBI-eight hour value using the Mann–Whitney U test. SEM, standard error of the mean; TBI, traumatic brain injury.

Back to article page