system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Aorta, Apoptosis, Calcium-Calmodulin-Dependent Protein Kinases, Cattle, Cells, Cultured, DNA Fragmentation, Drug Synergism, Endothelium, Vascular, Glucose, Hydrogen Peroxide, Oxidants.
user
Does high glucose enhance H2O2-induced apoptosis in bovine aortic endothelial cells? Context: To investigate the effect of high glucose on hydroperoxide (H2O2)-induced apoptosis in cultured bovine aortic endothelial cells (BAEC). BAEC were cultured and passaged in normal glucose (5.5 mmol.L-1, NG) and high glucose (25 mmol.L-1, HG). Morphologic changes and quantification of apoptotic cells were determined under fluorescence microscope after H2O2-treated BAEC for 24 h with Hoechst 33258 staining. DNA fragmentation was visualized by agarose gel electrophoresis. The expression of phospho-p38 Ca(2+)-calmodulin dependent protein kinase (CCDPK, formerly called MAPK) was measured by Western blotting. H2O2 elicited typical apoptotic morphologic changes (chromatic condensation, nucleus fragmentation). At 100 -300 mumol.L-1, both NG- and HG-BAEC incubated with H2O2 for 24 h increased cell apoptosis and phospho-p38 CCDPK expression in a concentration-dependent manner. In HG-BAEC, H2O2 induced DNA fragmentation at a lower concentration than that in NG-BAEC, and the apoptotic cell count in HG-BAEC was also higher than that of NG-BAEC (P < 0.05). Similarly, the expression of phospho-p38 CCDPK induced by H2O2 was up-regulated in HG-BAEC (P < 0.05).
assistant
High glucose enhances H2O2-induced apoptosis in BAEC, which is related to high expression of phospho-p38 CCDPK. Final Decision: yes