AICAR Sigma
AICAR Sigma
AICAR inhibits the growth of EGFR-activated cancer cell lines, including glioblastoma cells. (A) Western blot analysis demonstrated Akt Ser-473 phosphorylation in U87-EGFRvIII, but not U87 cells in response to repaying (1 nM) for 24 h. (B) Immunoblot analysis of effect of AICAR (0.5 mM) on Akt and mTORC1 signaling. U87-EGFRvIII cells were treated for up to 24 h and effect on signaling pathways was determined at indicated time points. We previously demonstrated that pharmacologic activation of AMP-activated protein kinas (AMPK) with 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR) 24 hours prior to (AICAR preconditioning; AICAR-PC) ischemia/reperfusion (I/R) prevents post ischemic leukocyte-endothelial cell adhesive interactions (LEI) by a mechanism initiated by endothelial nitric oxide syntheses (eNOS)-dependent NO production during the period of AICAR-PC.