Abstract
Total Panax notoginseng saponin (TPNS) is the main bioactivity compound derived from the roots and rhizomes of Panax notoginseng (Burk.) F.H. Chen. The aim of this study was to investigate the effectiveness of TPNS in treating vascular neointimal hyperplasia in rats and its mechanisms. Male Sprague-Dawley rats were randomly divided into five groups, sham (control), injury, and low, medium, and high dose TPNS (5, 10, and 20 mg/kg). An in vivo 2F Fogarty balloon-induced carotid artery injury model was established in rats. TPNS significantly and dose-dependently reduced balloon injury-induced neointimal area (NIA) (P<0.001, for all doses) and NIA/media area (MA) (P<0.030, for all doses) in the carotid artery of rats, and PCNA expression (P<0.001, all). The mRNA expression of smooth muscle (SM) α-actin was significantly increased in all TPNS groups (P<0.005, for all doses) and the protein expression was significantly increased in the medium (P=0.006) and high dose TPNS (P=0.002) groups compared to the injury group. All the TPNS doses significantly decreased the mRNA expression of c-fos (P<0.001). The medium and high dose TPNS groups significantly suppressed the upregulation of pERK1/2 protein in the NIA (P<0.025) and MA (P<0.004). TPNS dose-dependently inhibited balloon injury-induced activation of pERK/p38MAPK signaling in the carotid artery. TPNS could be a promising agent in inhibiting cell proliferation following vascular injuries.
Highlights
Vascular smooth muscle cells (VSMCs) are a major structural component of the vessel wall and play a key role in maintaining vascular structure
Compared to the injury group, Total Panax notoginseng saponin (TPNS) significantly alleviated the thickening of neointimal area (NIA), but it remained significantly greater than the sham group (Figure 1C)
The proliferation and migration of VSMC from the medial to the intima layer of the artery is a key early event and the main pathological process of vascular stenosis caused by neointima formation [22,23,24]
Summary
Vascular smooth muscle cells (VSMCs) are a major structural component of the vessel wall and play a key role in maintaining vascular structure. Vascular injury provokes neointimal hyperplasia and vessel remodeling by inducing aberrant VSMC proliferation and migration, which further reduces blood flow and aggravates vascular luminal narrowing and may result in cardiovascular disease [2,3]. Suppressing the proliferation and migration of VSMC could play an important role in preventing the pathological process of neointimal hyperplasia and might become a novel therapeutic strategy. There is a lack of effective drugs for controlling neointimal hyperplasia following vascular injury. A drug with an effective anti-neointimal function could be widely applied in clinical practice for the prevention and treatment of CHD and HTN, and other relevant diseases
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