Ang (1-7) protects islet endothelial cells from palmitate-induced apoptosis by AKT,eNOS,p38 MAPK,and JNK pathways

This study aimed to explore the effect of angiotensin (1-7) (ang (1-7)) on palmitate-induced apoptosis in islet endothelial cells and the mechanism of action. ms-1 cells were treated with palmitate in the presence or absence of ang (1-7). the percentage of apoptotic cells was determined by dna fragmentation and flow cytometry. reactive oxygen species (ros) production was measured using a reactive oxygen species assay kit. expression of akt,enos,c-jun n-terminal kinase (jnk),and p38 was detected by western blotting. compared with palmitate treated group,palmitate-induced apoptosis was decreased in ms-1 cells which were preincubated with ang (1-7) (p < 0.05). palmitate decreased the phosphorylation of akt and enos,and ang (1-7) increased the phosphorylation of these kinases (p < 0.05),with a concomitant reduction in ms-1 cells apoptosis. ang (1-7) also inhibited the palmitate-induced ros production and attenuated the apoptosis-related signaling molecule jnk and p38 activation (all p < 0.05). pi3k/akt,enos,p38 mapk,and jnk inhibitors blocked the antilipoapoptosis of ang (1-7) (all p < 0.05). our findings suggest that ang (1-7) reduces palmitate-induced islet endothelial cells apoptosis. akt/enos/no signaling and jnk and p38 pathway are involved in the ang (1-7)-mediated modulation of islet endothelial cells lipoapoptosis. © 2014 li yuan et al.