Related Experiment Video
Updated: Jan 25, 2026

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Ginsenoside Re inhibits PDGF-BB-induced VSMC proliferation via the eNOS/NO/cGMP pathway
Yang Gao1, Ping Zhu1, Shang-Fu Xu1
1Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, PR China.
Abstract:
Ginsenoside Re (GS-Re), which is a major monomeric member of the ginseng trialcohol saponin family, is one of the main active components of ginseng and plays an important role in protecting the cardiovascular system. Here, we report a novel function by which GS-Re regulates the eNOS/NO/cGMP pathway, which affects the platelet-derived growth factor-BB (PDGF-BB)-induced proliferation of vascular smooth muscle cells (VSMCs). GS-Re inhibited PDGF-BB-induced VSMC proliferation in a concentration-dependent manner without cytotoxicity, and the endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) antagonized the antiproliferative effect of GS-Re. The flow cytometry analysis suggested that GS-Re regulates VSMC proliferation by influencing the cell cycle transition from G0/G1 to S phase and decreasing the expression of G0/G1-specific regulatory proteins, including proliferating cell nuclear antigen (PCNA), cyclin D1, and CDK4, in PDGF-BB-treated VSMCs, consequently upregulating the protein expression of p21. After GS-Re treatment, the levels of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) and the phos-eNOS Ser1177/eNOS protein ratio were obviously increased. In addition, treatment with L-NAME blocked the eNOS/NO/cGMP signaling pathway, and the protein levels of PCNA, cyclin D1, and CDK4 were markedly increased in GS-Re-treated VSMCs, while p21 expression was decreased in PDGF-BB-induced VSMCs. Overall, these findings reveal that GS-Re can inhibit the proliferation of VSMCs through G0/G1 cell cycle arrest, which is closely related to eNOS/NO/cGMP pathway activation. The present results provide basic pharmacological evidence of the potential prevention and treatment of cardiovascular diseases by GS-Re.
Related Concept Videos
Feedback Inhibition
Abnormal Proliferation
C4 Pathway and CAM
C4 Pathway
The C4 pathway is used by plants such as...
Enzyme Inhibition
Other Glycolytic Pathways
Inhibition of Cdk Activity

