Involvement of Toll Like Receptor 2 Signaling in Secondary Injury during Experimental Diffuse Axonal Injury in Rats

Figure 10

TLR2 signaling pathway induced-inflammatory factors were involved in secondary injury after DAI. (a) Phosphorylation of signaling molecules including p38 MAPK, ERK1/2, and JNK in cortex was examined by western blotting. The expression of β-actin was used as an internal control. (b) The bar graphs showed the statistical results for phosphorylation levels of p38 MAPK, ERK1/2, and JNK. (c) Expression of NF-κB p65 and phospho-NF-κB p65 in nuclear extraction of cortex was examined by western blotting. The expression of lamin B was used as an internal control. (d) The bar graphs showed the statistical results for NF-κB p65 and phospho-NF-κB p65 in nuclear extraction. (e) The effects of TLR2 siRNA and Pam3CSK4 on the levels of inflammatory factors including TNF-α, IL-1β, and IL-6 in rat cortex after DAI were determined by ELISA. All data were presented as mean ± SD in three separate experiments ( = 6; < 0.05, compared with control group; < 0.05, compared with DAI 3 d group).

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