Notoginsenoside R1 inhibits vascular smooth muscle cell proliferation, migration and neointimal hyperplasia through PI3K/Akt signaling.
Haihong FangShilin YangYingying LuoCheng ZhangYi RaoRenjing LiuYulin FengJun YuPublished in: Scientific reports (2018)
Restenosis caused by neointimal hyperplasia significantly decreases long-term efficacy of percutaneous transluminal angioplasty (PTA), stenting, and by-pass surgery for managing coronary and peripheral arterial diseases. A major cause of pathological neointima formation is abnormal vascular smooth muscle cell (VSMC) proliferation and migration. Notoginsenoside R1 (NGR1) is a novel saponin that is derived from Panax notoginseng and has reported cardioprotective, neuroprotective and anti-inflammatory effects. However, its role in modulating VSMC neointima formation remains unexplored. Herein, we report that NGR1 inhibits serum-induced VSMC proliferation and migration by regulating VSMC actin cytoskeleton dynamics. Using a mouse femoral artery endothelium denudation model, we further demonstrate that systemic administration of NGR1 had a potent therapeutic effect in mice, significantly reducing neointimal hyperplasia following acute vessel injury. Mechanistically, we show that NGR1's mode of action is through inhibiting the activation of phosphatidylinositol 3-kinase (PI3K)/Akt signaling. Taken together, this study identified NGR1 as a potential therapeutic agent for combating restenosis after PTA in cardiovascular diseases.
Keyphrases
- smooth muscle
- pi k akt
- signaling pathway
- cell proliferation
- cell cycle arrest
- minimally invasive
- cardiovascular disease
- drug induced
- coronary artery
- coronary artery disease
- liver failure
- stem cells
- nitric oxide
- protein kinase
- cell cycle
- cell therapy
- type diabetes
- diabetic rats
- hepatitis b virus
- bone marrow
- cerebral ischemia
- endothelial cells
- extracorporeal membrane oxygenation
- mesenchymal stem cells
- acute respiratory distress syndrome
- percutaneous coronary intervention
- aortic dissection
- cardiovascular risk factors
- tyrosine kinase
- anti inflammatory
- atrial fibrillation
- cell migration