The Protective Effect of Notoginsenoside R1 on Vascular Endothelial Function in Atherosclerosis Models Mediated by the PI3K/AKT/NF-κB Pathway

Atherosclerosis (AS) is a prevalent cardiovascular disease characterized by lipid plaque formation in arterial walls, leading to vascular narrowing and impaired blood flow, which significantly affects patients' quality of life and can result in serious complications such as heart disease and stroke. Current treatments, including statins, have limitations, underscoring the urgent need for new therapeutic strategies. Notoginsenoside R1 (NR1) is the main active monomer of total Sanqi saponins and is effective in preventing and treating various cardiovascular diseases (such as ischemic heart disease, atherosclerosis, hypertension, and myocarditis). This study investigates the effects of NR1 on the viability of human umbilical vein endothelial cells (HUVECs) and its modulation of inflammatory factors, particularly through the PI3K/AKT/NF-κB signaling pathway. Employing a range of methodologies, including cell culture, CCK-8 assay, Griess assay, LDH release measurement, ELISA, and Western blot analysis, we assessed NR1's protective effects on endothelial cells. Results demonstrate that NR1 significantly enhances cell viability and reduces inflammatory factor levels, with an emphasis on its ability to inhibit the activation of the PI3K/AKT/NF-κB pathway. These findings suggest that NR1 could serve as a novel therapeutic agent in the treatment of atherosclerosis, providing a foundation for future clinical applications. Further research is warranted to explore the clinical implications of NR1 and its potential as a target for drug development in cardiovascular diseases.