Notoginsenoside Fc attenuates high glucose-induced vascular endothelial cell injury via upregulation of PPAR-γ in diabetic Sprague-Dawley rats.

Abstract

Endothelial injury from high glucose (HG) plays a dominant role in atherosclerosis, diabetes-induced vasculopathy, and vascular remodeling. Notoginsenoside Fc (Fc), a novel saponin isolated from P. notoginseng, has been shown to exhibit properties that counteract platelet aggregation. However, the potential roles and molecular mechanisms of Fc in preventing cardiovascular injury have yet to be explored. In this study, we present novel data that show the ability of Fc to prevent early atherosclerosis of diabetic Sprague-Dawley (SD) rats in vivo and to attenuate endothelial cell injury in vitro. Our results indicate that Fc protects rat aortic endothelial cells (RAOECs) from HG-induced injury by inhibiting apoptosis and promoting proliferation as well as by reducing endothelial cell production of pro-inflammatory cytokines: TNF-α, IL-1β, IL-6, ICAM-1. Furthermore, the downregulation of peroxisome proliferator-activated receptor-γ (PPAR-γ) in HG-challenged endothelial cells was prevented by Fc. Inhibition of PPAR-γ abrogated the effects of Fc on HG-induced pro-inflammatory cytokine production in RAOECs. These results indicate that Fc has a preventative effect on HG-induced endothelial cell injury partly through a PPARγ-mediated pathway, suggesting that Fc might provide a potential new therapeutic option for the treatment of diabetic vascular complications.

• Authors: Jingjing Liu, Chunyu Jiang, Xu Ma, Jianbo Wang
• Journal: Vascular pharmacology (Vascul Pharmacol) Vol. 109 Pg. 27-35 (10 2018) ISSN: 1879-3649 [Electronic] United States
• PMID: 29857059 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2018 Elsevier Inc. All rights reserved.

Chemical References

• Blood Glucose
• Cytokines
• Ginsenosides
• Inflammation Mediators
• PPAR gamma
• notoginsenoside Fc

Topics

• Animals
• Apoptosis (drug effects)
• Blood Glucose (metabolism)
• Cell Proliferation (drug effects)
• Cells, Cultured
• Cytokines (metabolism)
• Cytoprotection
• Diabetes Mellitus, Experimental (blood, drug therapy, pathology)
• Diabetic Angiopathies (blood, pathology, prevention & control)
• Dose-Response Relationship, Drug
• Endothelial Cells (drug effects, metabolism, pathology)
• Female
• Ginsenosides (pharmacology)
• Inflammation Mediators (metabolism)
• PPAR gamma (agonists, metabolism)
• Rats, Sprague-Dawley
• Signal Transduction (drug effects)
• Time Factors
• Up-Regulation