Likewise, induction of ER stress by tunicamycin impaired EDRs in conduit aortas which were rescued by PNS and PNE, and such improvement was abolished in the presence of Compound C. The present results show that both PNS and PNE effectively improved high glucose-induced endothelial dysfunction with alleviation of ER stress and oxidative stress through the AMPK/eNOS pathway. Here, NOS3 is linked to endothelial dysfunction.