Figure 3

IVIg treatment down regulates the expressions of the phosphorylated forms of TLR signalling cascade components. IVIg treatment down regulates the expressions of the phosphorylated forms of TLR signalling cascade components in cultured cortical neurons subjected to simulated ischemia. (A-E) Representative immunoblots and quantification illustrating increases in the levels of NF-κB-p-p65 and p-p38 MAPK in primary cortical neurons at indicated times during GD. Administration of IVIg (5 and 10 mg/ml) significantly attenuated the expression level of NF-κB-p-p65, p-JNK, p-p38 MAPK and p-c-Jun in GD 6-, 12- and 24-h-treated neurons. Data are represented as mean ± SEM. n = 5 cultures. ^* P < 0.05 in comparison with normal; ^** P < 0.01 in comparison with normal; ^*** P < 0.001 in comparison with normal; ⁺ P < 0.05 in comparison with vehicle-treated group; ⁺⁺ P < 0.01 in comparison with vehicle-treated group; ⁺⁺⁺ P < 0.001 in comparison with vehicle-treated group. (F-J) Representative immunoblots and quantification illustrating increases in the levels of NF-κB-p-p65 and p-p38 MAPK in primary cortical neurons at indicated times during OGD. Administration of IVIg (5 and 10 mg/ml) significantly attenuated the expression level of NF-κB-p-p65, p-JNK and p-p38 MAPK in OGD 6- and 12-h-treated neurons. Administration of 10 mg/ml IVIg significantly attenuated the expression level of p-c-Jun in OGD 6- and 12-h-treated neurons, however the effect of 5 mg/ml IVIg was significant at 12 but not 6 h of OGD. Data are represented as mean ± SEM. n = 5 cultures. ^* P < 0.05 in comparison with normal; ^*** P < 0.001 in comparison with normal; ⁺ P < 0.05 in comparison with vehicle-treated group; ⁺⁺ P < 0.01 in comparison with vehicle-treated group; ⁺⁺⁺ P < 0.001 in comparison with vehicle-treated group; ns, not significant.