Fig. 5. Analysis of the interaction between IB1/JIP1 and GLP-1R after tMCAO in rat. (A) IB1/JIP1 protein levels were down-regulated by 1 h tMCAO, and following reperfusion. Ex-4 treatment dramatically increased IB1/JIP1 levels in the rat brain, while ex9-39 did not. Up-regulation of IB1/JIP1 by ex-4 treatment led to reduced expression of phospho-JNK (n =4, ^#p<0.05, compared to chemical treated group at the same time point). (B) Endogenous IB1/JIP1 was captured by immunoprecipitation with an anti-IB1/JIP1 antibody in the total fraction of infarcted brain. Results were detected by immunoblotting using antibodies to GLP-1R, COX-2, and phospho-SAPK/JNK. Decreased GLP-1R was detected in the vehicle group, while the ex-4 treated group showed significant interactions between GLP-1R and IB1/JIP1 compared to the sham group. Input lysates showed no differences (n =4, ^*p<0.05, compared to sham-operated group, ^#p<0.01, compared to chemical-treated group).