作者机构：
[Deng, Chang-Qing; Chen, Gang] Hunan Univ Tradit Chinese Med, Pathophysiol Lab, Changsha, Hunan, Peoples R China.;[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, Pathophysiol Lab, Shaoshan Rd 113, Changsha, Hunan, Peoples R China.
通讯机构：
[Deng, Chang-Qing] H;Hunan Univ Tradit Chinese Med, Pathophysiol Lab, Shaoshan Rd 113, Changsha, Hunan, Peoples R China.
关键词：
BuYang HuanWu Decoction;Vascular smooth muscle cell;Platelet derived growth factor;Proliferating cell nuclear antigen;c-fos;CyclinD(1);Extracellular regulated protein kinases1/2;Mitogen-activated protein kinase;phosphatase-1
摘要：
Buyang Huanwu Decoction (BYHWD) was a commonly used traditional Chinese medicine for the treatment and prevention of ischemic cardiovascular and cerebral disease. Previous studies had shown that BYHWD alkaloids and glycosides could inhibit intimal hyperplasia and vascular smooth muscle cell (VSMC) proliferation after injury caused by balloon catheter. The present study aims to explore the mechanisms by which cell cycle was affected by BYHWD and its components. Primary rat VSMC was treated with platelet-derived growth factor (PDGF) and cell cycle phase and extracellular-signal regulated protein kinase (ERK) transduction pathway factors were measured. PDGF-treated cells were associated with a significant increase in the number of cells in the G(2)/M phase and S phase, and in the expression of P-ERK1/2, proliferating cell nuclear antigen (PCNA), c-fos, cyclinD(1) and cyclin-dependent kinase-4, as well as a decrease in the number of cells in the G(0)/C(1) phase, and in the expression of cyclin-dependent kinase inhibitor P21 protein and mitogen-activated protein kinase phosphatase-1 (MKP-1). Treatment with plasma of rats fed seven doses of BYHWD crude extract (22.2 g/kg), BYHWD alkaloids (1.66 g/kg), BYHWD glycosides (14.2 g/kg) or the negative control atorvastatin (20 mg/kg) inhibited these changes. All drug-containing plasma had similar activity to the mitogen activated protein kinase (MAPK)/ERK antagonist PD098059 which inhibited PDGF-induced expression of P-ERK1/2 and enhanced MKP-1. These suggest that BYHWD and its components may prevent VSMC proliferation by interfering with the ERK transduction pathway. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
摘要：
AIM: To investigate the effect of Simotang (Decoction of Four Powered Drugs) on gastrointestinal motility, motilin and cholecystokinin expression in chronically stressed mice. METHODS: Forty mice were randomly divided into control group, stress group (model group), mosapride group and Simotang group, 10 in each group. A variety of unpredictable stimulations were used to induce chronic stress in mice. Then, the mice were treated with distilled water, mosapride or Simotang for 7 d. Gastric emptying and intestinal propulsion function were detected. Serum level of motilin was measured by enzyme-linked immunosorbent assay. Expression of cholecystokinin (CCK) in intestine, spinal cord and brain of mice was detected by immunohistochemistry and semi-quantitative reverse transcription polymerase chain reaction, respectively. RESULTS: Simotang improved the gastric emptying and intestinal propulsion in chronically stressed mice. Furthermore, the serum motilin level was significantly higher and the expression levels of CCK-positive cells and genes were significantly lower in intestine, spinal cord and brain of Simotang group than in those of model group (P < 0.05). No significant difference was found in serum motilin level and expression levels of CCK-positive cells and genes between the mosapride and Simotang groups. CONCLUSION: Simotang enhances the gastrointestinal motility in chronically stressed mice by regulating the serum motilin level and the expression of cholecystokinin
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.
摘要：
Atherosclerosis is characterized by a chronic inflammatory condition that involves numerous cellular and molecular inflammatory components. A wide array of inflammatory mediators, such as cytokines and proteins produced by macrophages and other cells, play a critical role in the development and progression of the disease. ATP-binding membrane cassette transporter A1 (ABCA1) is crucial for cellular cholesterol efflux and reverse cholesterol transport (RCT) and is also identified as an important target in antiatherosclerosis treatment. Evidence from several recent studies indicates that inflammation, along with other atherogenic-related mediators, plays distinct regulating roles in ABCA1 expression. Proatherogenic cytokines such as interferon (IFN)-γ and interleukin (IL)-1β have been shown to inhibit the expression of ABCA1, while antiatherogenic cytokines, including IL-10 and transforming growth factor (TGF)-β1, have been shown to promote the expression of ABCA1. Moreover, some cytokines such as tumor necrosis factor (TNF)-α seem to regulate ABCA1 expression in species-specific and dose-dependent manners. Inflammatory proteins such as C-reactive protein (CRP) and cyclooxygenase (COX)-2 are likely to inhibit ABCA1 expression during inflammation, and inflammation induced by lipopolysaccharide (LPS) was also found to block the expression of ABCA1. Interestingly, recent experiments revealed ABCA1 can function as an antiinflammatory receptor to suppress the expression of inflammatory factors, suggesting that ABCA1 may be the molecular basis for the interaction between inflammation and RCT. This review aims to summarize recent findings on the role of inflammatory cytokines, inflammatory proteins, inflammatory lipids, and the endotoxin-mediated inflammatory process in expression of ABCA1. Also covered is the current understanding of the function of ABCA1 in modulating the immune response and inflammation through its direct and indirect antiinflammatory mechanisms including lipid transport, high-density lipoprotein (HDL) formation and apoptosis.
摘要：
Cholesterol efflux from lipid-loaded cells is a key athero-protective event that counteracts cholesterol uptake. The imbalance between cholesterol efflux and uptake determines the prevention or development of atherosclerosis. Many proteins and factors participate in the cholesterol efflux event. However, there are currently no systematic models of reverse cholesterol transport (RCT) that include most RCT-related factors and events. On the basis of recent research findings from other and our laboratories, we propose a novel model of one center and four systems with coupling transportation and networking regulation. This model represents a common way of cholesterol efflux; however, the systems in the model consist of different proteins/factors in different cells. In this review, we evaluate the novel model in vascular smooth muscle cells (VSMCs) and macrophages, which are the most important original cells of foam cells. This novel model consists of 1) a caveolae transport center, 2) an intracellular trafficking system of the caveolin-1 complex, 3) a transmembrane transport system of the ABC-A1 complex, 4) a transmembrane transport system of the SR-B1 complex, and 5) an extracelluar trafficking system of HDL/Apo-A1. In brief, the caveolin-1 system transports cholesterol from intracellular compartments to caveolae. Subsequently, both ABC-A1 and SR-B1 complex systems transfer cholesterol from caveolae to extracellular HDL/Apo-A1. The four systems are linked by a regulatory network. This model provides a simple and concise way to understand the dynamic process of atherosclerosis.
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
