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Fig. 4. Attenuation of the SAPK/JNK pathway by ex-4 through the GLP-1R. (A) Phosphorylation of SAPK/JNK was elevated following ischemic reperfusion injury in rats. Treatment with ex-4 prior to 1 h transient middle cerebral artery occlusion inhibited up-regulation of phospho-JNK and COX-2, while treatment with ex-9-39 increased phospho-JNK levels. Ex-4 did not significantly change other MAPK signaling. (B) Quantitative analyses showed significant augmentation in JNK-mediated COX-2 expression in rat (n =4, **p<0.01, ***p<0.001, compared to sham-operated group, ##p<0.01, compared to chemical-treated group at the same time point).
Exp Neurobiol 2017;26:227~239
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