['Previous studies showed that homocysteine(Hcy) could injure vascular endothelial cells via several mechanisms, including its promotion of oxidative stress pathway and endoplasmic reticulum stress (ER-stress) pathway. Salidroside(SAL) is an active component of Rhodiola rosea with documented antioxidative properties. Emerging evidence conformed that SAL attenuated Hcy induced endothelial dysfunction by reducing oxidative stress. However, its role in ER-stress pathway remains un-clarified.', 'The purpose of this study is to explore the mechanism of the protective effect of SAL on Hcy induced endothelial dysfunction.', 'Pretreatment of the human umbilical vein endothelial cells (HUVECs) with SAL significantly reduced the cell damage effects brought by Hcy in a dose-dependent manner. Functional studies on the HUVECs found that SAL rescued the endoplasmic reticulum stress induced by Hcy. The underlying mechanisms involve the inhibition of Hcy-induced activation of binding protein (Bip) and C/EBP homologous protein (CHOP), as well as the phosphorylation of protein kinase RNA-like ER kinase (PERK) or inositol-requiring enzyme 1 alpha (IRE1α).'] Does salidroside protect against Homocysteine-induced Injury in HUVECs via The Regulation of Endoplasmic Reticulum Stress?