ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Salidroside Protects Against Advanced Glycation End Products-Induced Vascular Endothelial Dysfunction.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Cepharanthine alleviated chronic prostatitis/chronic pelvic pain syndrome by activating Nrf2 and inhibiting the NF-κB pathway.Biology direct · 2026Article
- Natural Nrf2 activators modulate antioxidant gene expression and apoptosis in leukemic K-562 cells.Medical oncology (Northwood, London, England) · 2025Article
- Network pharmacology-based study in polymetformin's new function of blocking ages/rage pathway curing diabetic complications.Scientific reports · 2025Article
- Salidroside Reduced CaCell biochemistry and biophysics · 2024Article
- Advance on Chinese Medicine for Hypertensive Renal Damage: Focus on the Complex Molecular Mechanisms.Chinese journal of integrative medicine · 2024Review
- Extracellular vesicles derived from fibroblasts induced with or without high glucose exert opposite effects on wound healing and angiogenesis.Frontiers in surgery · 2022Article
- Activation of Nrf2/HO-1 signaling: An important molecular mechanism of herbal medicine in the treatment of atherosclerosisJournal of advanced research · 2021Review
- Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy.BMC complementary medicine and therapies · 2021Article
- The Role of Adaptogens in Prophylaxis and Treatment of Viral Respiratory Infections.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Glycolaldehyde-modified proteins cause adverse functional and structural aortic remodeling leading to cardiac pressure overload.Scientific reports · 2020Article
- Salidroside inhibits platelet function and thrombus formation through AKT/GSK3β signaling pathway.Aging · 2020Article
- Antioxidant Effects of Salidroside in the Cardiovascular System.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Beneficial Effects of Rhodiola and Salidroside in Diabetes: Potential Role of AMP-Activated Protein Kinase.Molecular diagnosis & therapy · 2019Review
- Salidroside attenuates oxidized low‑density lipoprotein‑induced endothelial cell injury via promotion of the AMPK/SIRT1 pathway.International journal of molecular medicine · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 AND 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-κB) 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-κB p65.
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