Figure 2

ABL decreases inflammatory responses via inhibiting the TLR4/NF-κB signaling cascades. (A) Total proteins were extracted from brain tissues of sham, MCAO and MCAO + ABL-treated mice and analyzed by Western blotting for TLR4, NF-κB, I-κB, MyD88, SOCS1 and TAB2, and band intensities that were normalized to β-actin are represented by bar graphs as the means ± SD (n = 6 per group), *P < 0.05 versus sham group; #P < 0.05 versus MCAO group. (B) Immunohistochemical staining for NF-κB and TLR4 in brain tissues of sham, MCAO, and MCAO + ABL-treated groups. Scale bar = 20 µmol/L. Bars represent the number of NF-κB- and TLR4-positive cells. n = 5 per group; *P < 0.05 versus sham group; #P < 0.05 versus MCAO group. (C) BV2 cells were treated with or without ABL (100 µmol/L) for 24 h prior to OGD. TLR4, NF-κB, I-κB, MyD88, SOCS1 and TAB2 were detected by Western blotting, and band intensities that were normalized to β-actin are represented by bar graphs as the means ± SD from three independent experiments; *P< 0.05 versus con group; ^#P< 0.05 versus OGD group.