Fig. 4

Oridonin improves LSS induced EC dysfunction and oxidative stress by activating NRF2. A Results of the fluorescent probe DAF-FM diacetate revealed that oridonin treatment increased the LSS-induced reduced NO activity by activating NRF2. B Oridonin treatment decreased the LSS-induced upregulation in ET-1 mRNA expression levels. C Oridonin treatment increased the LSS-induced downregulation in eNOS mRNA expression levels. D Oridonin treatment increased the LSS-induced downregulation in PGIS mRNA expression levels. E Results of the fluorescent probe dye DHE illustrated that oridonin treatment attenuated the LSS-induced increase in ROS activity in EA.hy926 cells. F Oridonin treatment increased the LSS-induced decrease in SOD activity in EA.hy926 cells. G Oridonin treatment decreased the LSS-induced increase in MDA content in EA.hy926 cells. H Oridonin treatment decreased the LSS-induced increase in GSSG content in EA.hy926 cells. I Oridonin treatment increased the LSS-induced decrease in GSH content in EA.hy926 cells. ^##P < 0.01 vs. LSS (−) + oridonin (−) + NRF2 siRNA (−); ^**P < 0.01 vs. LSS (+) + oridonin (−) + NRF2 siRNA (−); ^$$P < 0.01 vs. LSS (+) + oridonin (+) + NRF2 siRNA (−). LSS, low shear stress; NRF2, nuclear factor erythroid 2-related factor 2; ET-1, endothelin-1; eNOS, endothelial nitric oxide synthase; PGIS, prostaglandin synthase; ROS, reactive oxygen species; SOD, superoxide dismutase; MDA, malondialdehyde; GSSG, glutathione disulfide; GSH, glutathione; siRNA, small interfering RNA