Skip to main content
Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: Valproic acid attenuates traumatic spinal cord injury-induced inflammation via STAT1 and NF-κB pathway dependent of HDAC3

Fig. 7

VPA treatment suppressed the NF-κB pathway via elevating STAT1 expression in the lesioned spinal cord 7 days after SCI. a Co-IP analysis showed a greater elevation in the STAT1 after the VPA treatment than in the SCI group (P < 0.05). b Co-IP analysis showed a greater elevation in the NF-κB acetylation after the VPA treatment than in the SCI group (P < 0.05). c The acetylated STAT1 formed a complex with the nuclear NF-κB p65. The VPA induced significant interactions between STAT1 and NF-κB p65 after the SCI (P < 0.05). d Significantly, less NF-κB p65 DNA-binding activity was observed in the SCI + VPA group than in the SCI group. e The VPA treatment inhibited NF-κB p65 nuclear translocation and expression (P < 0.05). f The inhibitory effect of the VPA treatment on the neuroinflammatory response was reversed by the pharmacological inhibition of STAT1 (fludarabine, flu). g The inhibitory effect of the VPA treatment on the NF-κB pathway was reversed by pharmacological inhibition of STAT1. Values were expressed as mean ± standard deviation (n = 6 per group). N.S., P > 0.05, *P < 0.05, **P < 0.01

Back to article page