Salidroside Protects Against Advanced Glycation End Products-Induced Vascular Endothelial Dysfunction

Background: Salidroside, the major active compound in Rhodiola, has been reported to provide beneficial effects on cardiovascular diseases, but its effects on diabetes-induced vascular endothelial dysfunction are less known. Here, we examined the protective effects of salidroside on endothelial function in diabetes and explored the potential underlying mechanism. Material/Methods: First, we assessed the endothelium-dependent relaxation response to acetylcholine, with or without salidroside treatment, in aortas isolated from Sprague-Dawley rats. Then, cell viability, oxidative biomarkers, and protein expression were tested to determine the effect of salidroside treatment on human umbilical vein endothelial cells (HUVECs) in vitro. Results: Advanced glycation end product (AGE)-induced endothelial dysfunction was significantly improved by salidroside treatment (P<0.05), as shown by a reduced relaxation response to the vasodilator acetylcholine. Further, incubation with salidroside restored NO levels and reduced reactive oxygen species formation in AGE-stimulated HUVECs in a concentration-dependent manner (P<0.05). We also showed that nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase 1 (HO-1) and nuclear factor kappa B (NF-kappa B) signaling was critical for the salidroside-mediated beneficial regulation. Conclusions: Our results demonstrate that salidroside protects against AGE-induced endothelial dysfunction, and its effects may be in part attributed to the induction of HO-1 and attenuation of phosphorylated NF-kappa B p65.