Effects of zinc and manganese on advanced glycation end products (AGEs) formation and AGEs-mediated endothelial cell dysfunction.

摘要: Abstract Aims The present study investigated the effects of ZnCl 2 and MnCl supplementations on advanced glycation end products (AGEs) formation AGEs-mediated endothelial cell dysfunction. Main methods Fluorescence detection was used to monitor Maillard reaction. Inductively coupled plasma optical emission spectroscopy test cellular zinc manganese levels. Real-time reverse transcription polymerase chain reaction western blot were analyze expression nitric oxide synthase (eNOS), nuclear factor kappa B (NF-κB), receptor for AGEs (RAGE). Intracellular reactive oxygen species (ROS) (NO) production, NOS activity determined by fluorescent probe assay, superoxide dismutase (SOD) water soluble tetrazolium salt assay. Key findings showed excellent inhibitory effect formation. Primary cultured bovine aortic cells (BAECs) exposed 30 min, followed trace element treatments. Cell viability levels declined due exposure, which improved with . Furthermore, supplementation effectively enhanced intracellular NO elevated eNOS enzymatic activity, down-regulated NF-κB activation RAGE expression. dose-dependently impaired ROS formation, protein translocation, as well restored Mn-SOD capability. Significance Our suggested that elements relevant diabetic, such played different roles in AGEs. Both benefited AGEs-injured BAECs through mechanisms.