Chen JS et al. – Long–term presence of high glucose induced STAT3 mediated ICAM–1 dependent endothelial adhesiveness to monocytes via the osmotic–related redox–dependent interleukin–6 pathways. GBE reduced high–glucose–induced endothelial inflammation mainly by inhibiting interleukin–6 activation. Future study is indicated to validate the antioxidant/anti–inflammatory strategy targeting on interleukin–6 for endothelial protection in in vivo and clinical hyperglycemia. [more...]