作者机构：
[Wu, Lu] Hunan Univ Tradit Chinese Med, Affiliated Tradit & Western Med Hosp 2, Changsha, Hunan, Peoples R China.;[Deng, Chang-Qing] Hunan Univ Tradit Chinese Med, Sch Integrated Chinese & Western Med, Pathophysiol Lab, Changsha, Hunan, Peoples R China.;[Tang, Ying-Hong] Hunan Univ Tradit Chinese Med, Dept Pharmacol, Changsha, Hunan, Peoples R China.;[Li, Hua; Zhang, Guo-Min; Chen, Bei-Yang] Hunan Univ Tradit Chinese Med, Dept Pathol, Changsha, Hunan, Peoples R China.;[Deng, Chang-Qing] Hunan Univ Tradit Chinese Med, Sch Integrated Chinese & Western Med, Pathophysiol Lab, Xiangzui Rd, Changsha, Hunan, Peoples R China.
通讯机构：
[Deng, Chang-Qing] H;Hunan Univ Tradit Chinese Med, Sch Integrated Chinese & Western Med, Pathophysiol Lab, Xiangzui Rd, Changsha, Hunan, Peoples R China.
关键词：
Total saponins of "panax notoginseng root";Atorvastatin;Vascular smooth muscle cell;Proliferating cell nuclear antigen;Cyclind D-1;Cycline;Extracellular matrix;Collagen I;Fibronectin;Matrix metalloproteinase-9;Tissue inhibitor metalloproteinase-1
摘要：
Aim of the study: the effect of total saponins of "panax notoginseng root" on aortic intimal hyperplasia and the expressions of cell cycle protein and extracellular matrix in rats Materials and methods: Sprague-Dawley rats were randomly divided into sham-operated, control, TSPN and atorvastatin group. Rat aorta intima in all groups were injured by insertion of domestic balloon catheter into the aortae except sham-operated rats. Drugs were administrated orally from the second day after vascular injury and continued for 14 days. The injured segments of aortae were collected on the sixteenth day after operation to observe the morphological changes of vascular structure and to examine the expressions of proliferating cell nuclear antigen(PCNA), cyclinD1, cyclinE, collagen I(Col-I), fibronect(FN), matrix metalloproteinase-9(MMP-9) and tissue inhibitor metalloproteinase-1(TIMP-1). Results: TPNS significantly inhibited the vascular intimal hyperplasia. TPNS significantly lowered the expression of PCNA, cyclinE, cyclinD1, FN and MMP-9. TPNS had no significant impacts on the expression of Col-I and TIMP-1. Conclusions: Our studies indicated that TSPN could inhibit vessel restenosis after vascular intimal injury, and its mechanisms may be related to the blockage of the excessive proliferation of VSMC, the reduction of ECM protein deposition in the endometrium, and the degradation of ECM protein. (C) 2009 Elsevier GmbH. All rights reserved.
作者机构：
[Li, Hua; Chen, Bei-Yang] Hunan Univ Tradit Chinese Med, Dept Histol & Embryol, Changsha, Hunan, Peoples R China.;[Deng, Chang-Qing; Zhang, Shu-Ping; Liang, Yan] Hunan Univ Tradit Chinese Med, Lab Pathophysiol, Changsha, Hunan, Peoples R China.;[Li, Hua; Luo, Xue-Gang] Cent S Univ, Xiangya Sch Med, Dept Anat & Neurobiol, Changsha, Hunan, Peoples R China.
通讯机构：
[Deng, Chang-Qing] H;Hunan Univ Tradit Chinese Med, Lab Pathophysiol, Changsha, Hunan, Peoples R China.
关键词：
Total saponins of Panax notoginseng;Cerebral ischemia-reperfusion;TUNEL;Caspase-1;Caspase-3;Caspase-8
摘要：
Ethnopharmacological relevance: Total saponins of Panax notoginseng (TSPN), main constituents extracted from Panax Notoginseng, a highly valued traditional Chinese medicine, have been shown to be an effective agent on cerebral infarction. Aim of the study: The effects of TSPN on apoptosis and expressions of caspase-1, caspase-3 and caspase-8 were studied after cerebral ischemia for 2 h followed by reperfusion for 46 h in rats. Materials and methods: Rats were subjected to transient middle cerebral artery occlusion (MCAO) model using the intraluminal thread. TSPN was administered intraperitoneally at 5 min before and 12 h, 24 h and 36 h after MCAO, respectively. Results: TSPN (at the dose of 25 mg/kg) significantly attenuated TUNEL-positive cells and reduced the expression of caspase-1 and caspase-3 compared to the model group, while it had no obvious effect on the expression of caspase-8. Conclusions: The neuroprotective effect of TSPN on focal ischemia may be related to inhibition of apoptosis and caspases activation. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
作者机构：
[李花] Department of Histology and Embryology, Hunan University of Traditional Chinese Medicine, Changsha 410208, Hunan Province, China;Laboratory of Pathophysiology, Hunan University of Traditional Chinese Medicine, Changsha 410208, Hunan Province, China
通讯机构：
Laboratory of Pathophysiology, Hunan University of Traditional Chinese Medicine, China
摘要：
Aim of the study: The inhibitive effect of BuYang HuanWu Decoction (BYHWD) and its major components on vascular intimal hyperplasia and the expressions of cell cycle protein and extracellular matrix protein. Materials and methods: Sprague-Dawley rats were randomly divided into sham-operated, control, alkaloid, glycoside, BYHWD and atorvastatin groups. Rat aorta intima in all groups were injured by insesion of domestic balloon catheter into the aortae except sham-operated rats. Drugs were administrated orally from the second day after vascular injury and continued for 14 days. The injured segments of aortae were collected on the sixteenth day after operation to observe the morphological changes of vascular structure and to examine the expressions of proteins in vascular cells associated with cell cycle including proliferating cell nuclear antigen(PCNA), cyclinD(1) and cyclinE, and extracellular matrix(ECM) proteins including collagen I (Col-1) and fibronectin (FN), further to discover the involved biologically active substances and the potential mechanisms. Results: Alkaloid and glycosid isolated from BYHWD were more effective than BYHVVD in the inhibition of intimal hyperplasia and the expressions of PCNA, cyclinD(1), cychnE, Col-I and FN, suggesting that alkaloid and glycoside may be the main components of BYHWD responsible for the observed inhibition of excessive hyperplasia of vascular intima. Conclusions: The mechanism associated with the anti-hyperplasia activity of BYHVVD and its effective components may be related to the blockage of cell cycles of VSMC, and the inhibition of the ECM protein synthesis, even the increased degradation of ECM proteins. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
