| Objective:To investigate the protective effect of Ang 1–7 against ox-LDL –induced endoplasmic reticulum stress(ERS) and apoptosis via Mas Receptor in Human umbilical vein endothelial cells(HUVECs),and provide a potential therapeutic strategy that the Ang 1-7/Mas receptor axis to treat ox-LDL-induced cardiovascular diseases related to ER stress.Methods:HUVECs were cultured in 1640 medium containing 12% fetal bovine serum,1%penicillin and streptomycin. After 50% confluence was obtained, they were treated medium without FBS for 12 h, and later were replaced with new complete media,Experiment was divided into five groups: the control group; the ox-LDL group:cells were exposed to ox-LDL(75mg/L)30 min; the Ang-(1-7)+ ox-LDL group: cells were exposed to Ang-(1-7)(1000nmol/L)30 min before exposure to ox-LDL(75mg/L)for 24 h; the A-779 +Ang-(1-7)+ ox-LDL group: cells were exposed to A-779(1000nmol/L)30 min before exposure to Ang-(1-7)(1000nmol/L)for 30 min,and after1 h were replaced with ox-LDL(75mg/L)for 24 h. the A-779 + ox-LDL group: cells were exposed to A-779(1000nmol/L)30 min before exposure to ox-LDL(75mg/L)for 24 h. We performed the following experimental procedures: RT-q PCR, caspase-3,Tunel and Western blot analysis.Results:The expression of ER stress proteins were elevated by ox-LDL in HUVECs. This elevation was reversed by co-incubation with Ang 1–7 while the presence of A779 antagonized the effect of Ang 1–7. Ox-LDL-induced increase in the m RNA expression of CHOP and GRP78(ER chaperones) was also inhibited by Ang 1–7, which was again antagonized by A779. Likewise, ox-LDL-treated HUVECs exhibited an elevated apoptosis, which was blunted by co-treatment with Ang 1–7 and the latter effect was reversed by A779.Conclusion:Ox-LDL-stimulated ER stress contributes to endothelial apoptosis. Ang-(1–7)protects against ox-LDL-Induced Endothelial Endoplasmic Reticulum Stress and apoptosis is most likely mediated via Mas receptor... |
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