Effect of Panax notoginseng saponins on vascular intima hyperplasia and PCNA expression in rat aorta after balloon angioplasty.
- Author:
Jianling WANG
1
;
Lu WU
;
Wei ZHANG
;
Changqing DENG
Author Information
- Publication Type:Journal Article
- MeSH: Angioplasty, Balloon, Coronary; Animals; Aorta; drug effects; metabolism; pathology; Cell Proliferation; drug effects; Gene Expression Regulation; drug effects; Hyperplasia; drug therapy; metabolism; pathology; therapy; Male; Panax notoginseng; chemistry; Proliferating Cell Nuclear Antigen; metabolism; Rats; Saponins; administration & dosage; pharmacology; therapeutic use; Tunica Intima; drug effects; metabolism; pathology
- From: China Journal of Chinese Materia Medica 2009;34(6):735-739
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect and the mechanism of panax notoginseng saponins (PNS) on the vascular intima hyperplasia and expression of proliferating cell nuclear antigen (PCNA) after aortic intima injury induced ballcon in rats.
METHODModel of aortic intima denudation in rats was established by 2.0 forgarty. The rats were randomly divided into sham group, model group, PNS group and atorvastatin group. Drugs were administered at the second day after the aortic intima injury for 14 days. The injured thoracic aorta segment were taken to detected the vascular morphological changes and expression of PCNA by histomorphology and immunohistochemic methods.
RESULTThe intimal area (IA), intimal thickness (IT), hyperplasia ratio of intimal area (HRIA), the ratio of intimal/mesolamella area and thickness in the model group were significantly higher than those of the sham operation (P<0.01). The above indexes in PNS and atorvastatin group were markedly lower than those in the model group (P<0.05). Compared with the sham group, the expression of PCNA in the model was enhanced remarkably (P<0.01). Compared with the model group, the expression of PCNA in PNS and atorvastatin group was significantly lowered (P<0.01).
CONCLUSIONPNS could inhibit intima hyperplasia by inhibiting proliferation of the vascular smooth muscle cell after vascular intima injury.
