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Fig. 2. Neuroprotective effects of ex-4 through the G protein-coupled GLP-1 receptor. (A) Infarct volume was assessed by TTC staining after tMCAO in rats. Treatment with ex-4, GLP-1R agonist, resulted in a significant reduction of brain tissue damage after ischemic injury. Ex9-39, a GLP-1R antagonist, reduced brain infarction volume; however, it was less than that of ex-4 (n =3, **p<0.01, ***p<0.001, compared to sham-operated group, ##p<0.01, ###p<0.001, compared to each chemical-treated group). (B) Reduction of GLP-1R protein and mRNA expression were noted at 48 h after 1 h MCAO. Ex-4 efficiently counteracted decreases in GLP-1R in the ischemic rat brain. Treatment of ex9-39 reduced the level of GLP-1R as much as the vehicle group. Ischemic reperfusion injury significantly increased GLP-1 levels (n =5, *p<0.05, ***p<0.001, compared to sham-operated group, #p<0.05, ##p<0.01, compared to each chemical-treated group). (C) In primary neurons, mouse brain microglia cells, and endothelial cells, ex-4 increased the reduced GLP-1R protein levels after OGD compared to the vehicle group (n =5, **p<0.01, compared to Nor, ##p<0.01, compared to each chemical-treated group). (D) Cyclic AMP levels were evaluated to investigate GLP-1R signaling. Cyclic AMP levels were decreased after 1 h tMCAO, but showed a significant increase in the ex-4 treated animal group (n =4, ##p<0.01, compared to vehicle group).
Exp Neurobiol 2017;26:227~239
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