Figure 6

IVIg treatment prevents an increased expression level of the phosphorylated forms of TLR signalling cascade components. IVIg treatment prevents an increased expression level of the phosphorylated forms of TLR signalling cascade components in vivo following stroke. (A-E) Representative immunoblots and quantification illustrating increases in the levels of NF-κB-p-p65, p-JNK, p-p38 MAPK and p-c-Jun in ipsilateral brain tissues of C57BL/6 J mice following MCAO (1 h) and reperfusion (6 and 24 h). Administration of IVIg (1 g/kg) significantly prevents the increased expression levels of NF-κB-p-p65, p-JNK, p-p38 MAPK and p-c-Jun following stroke. Data are represented as mean ± SEM. n = 5 to 6 animals in each group. ^# P < 0.05 in comparison with sham; ^## P < 0.01 in comparison with sham; ^### P < 0.001 in comparison with sham; *P < 0.05 in comparison with I/R 6; **P < 0.01 in comparison with I/R 6; ***P < 0.001 in comparison with I/R 6; ⁺ P < 0.05 in comparison with I/R 24; ⁺⁺ P < 0.01 in comparison with I/R 24; ⁺⁺⁺ P < 0.001 in comparison with I/R 24. (F, G) Representative immunoblots and quantification illustrating decrease in the levels of anti-apoptotic Bcl-2 in ipsilateral brain tissues of C57BL/6 J mice following MCAO (1 h) and reperfusion (6 and 24 h). Administration of IVIg (1 g/kg) significantly prevents a decreased level of Bcl-2 following stroke. Data are represented as mean ± SEM. n = 5 to 6 animals in each group. ^### P < 0.001 in comparison with sham; *P < 0.05 in comparison with I/R 6; ⁺⁺⁺ P < 0.001 in comparison with I/R 24.