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学者姓名:臧伟进

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< Page ,Total 28 >
Pyridostigmine protects against cardiomyopathy associated with adipose tissue browning and improvement of vagal activity in high-fat diet rats SCIE PubMed Scopus
期刊论文 | 2018 , 1864 (4) , 1037-1050 | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
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Abstract :

Obesity, a major contributor to the development of cardiovascular diseases, is associated with an autonomic imbalance characterized by sympathetic hyperactivity and diminished vagal activity. Vagal activation plays important roles in weight loss and improvement of cardiac function. Pyridostigmine is a reversible acetylcholinesterase inhibitor, but whether it ameliorates cardiac lipid accumulation and cardiac remodeling in rats fed a high-fat diet has not been determined. This study investigated the effects of pyridostigmine on high-fat diet induced cardiac dysfunction and explored the potential mechanisms. Rats were fed a normal or high-fat diet and treated with pyridostigmine. Vagal discharge was evaluated using the BL-420S system, and cardiac function by echocardiograms. Lipid deposition and cardiac remodeling were determined histologically. Lipid utility was assessed by qPCR. A high-fat diet led to a significant reduction in vagal discharge and lipid utility and a marked increase in lipid accumulation, cardiac remodeling, and cardiac dysfunction. Pyridostigmine improved vagal activity and lipid metabolism disorder and cardiac remodeling, accompanied by an improvement of cardiac function in high-fat diet-fed rats. An increase in the browning of white adipose tissue in pyridostigmine-treated rats was also observed and linked to the expression of UCP-1 and CIDEA. Additionally, pyridostigmine facilitated activation of brown adipose tissue via activation of the SIRT-1/AMPK/PGC-l alpha pathway. In conclusion, a high-fat diet resulted in cardiac lipid accumulation, cardiac remodeling, and a significant decrease in vagal discharge. Pyridostigmine ameliorated cardiomyopathy, an effect related to reduced cardiac lipid accumulation, and facilitated the browning of white adipose tissue while activating brown adipose tissue.

Keyword :

Obesity Adipose tissue Cardiac remodeling Cardiac lipid accumulation Pyridostigmine

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GB/T 7714 Lu, Yi , Wu, Qing , Liu, Long-Zhu et al. Pyridostigmine protects against cardiomyopathy associated with adipose tissue browning and improvement of vagal activity in high-fat diet rats [J]. | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE , 2018 , 1864 (4) : 1037-1050 .
MLA Lu, Yi et al. "Pyridostigmine protects against cardiomyopathy associated with adipose tissue browning and improvement of vagal activity in high-fat diet rats" . | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE 1864 . 4 (2018) : 1037-1050 .
APA Lu, Yi , Wu, Qing , Liu, Long-Zhu , Yu, Xiao-Jiang , Liu, Jin-Jun , Li, Man-Xiang et al. Pyridostigmine protects against cardiomyopathy associated with adipose tissue browning and improvement of vagal activity in high-fat diet rats . | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE , 2018 , 1864 (4) , 1037-1050 .
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Vagal nerve stimulation improves mitochondrial dynamics via an M-3 receptor/CaMKK/AMPK pathway in isoproterenol-induced myocardial ischaemia SCIE PubMed Scopus
期刊论文 | 2017 , 21 (1) , 58-71 | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | IF: 4.302
WoS CC Cited Count: 12
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Mitochondrial dynamicsfission and fusionare associated with ischaemic heart disease (IHD). This study explored the protective effect of vagal nerve stimulation (VNS) against isoproterenol (ISO)-induced myocardial ischaemia in a rat model and tested whether VNS plays a role in preventing disorders of mitochondrial dynamics and function. Isoproterenol not only caused cardiac injury but also increased the expression of mitochondrial fission proteins [dynamin-related peptide1 (Drp1) and mitochondrial fission protein1 (Fis-1)) and decreased the expression of fusion proteins (optic atrophy-1 (OPA1) and mitofusins1/2 (Mfn1/2)], thereby disrupting mitochondrial dynamics and leading to increase in mitochondrial fragments. Interestingly, VNS restored mitochondrial dynamics through regulation of Drp1, Fis-1, OPA1 and Mfn1/2; enhanced ATP content and mitochondrial membrane potential; reduced mitochondrial permeability transition pore (MPTP) opening; and improved mitochondrial ultrastructure and size. Furthermore, VNS reduced the size of the myocardial infarction and ameliorated cardiomyocyte apoptosis and cardiac dysfunction induced by ISO. Moreover, VNS activated AMP-activated protein kinase (AMPK), which was accompanied by phosphorylation of Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) during myocardial ischaemia. Treatment with subtype-3 of muscarinic acetylcholine receptor (M3R) antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide or AMPK inhibitor Compound C abolished the protective effects of VNS on mitochondrial dynamics and function, suggesting that M3R/CaMKK/AMPK signalling are involved in mediating beneficial effects of VNS. This study demonstrates that VNS modulates mitochondrial dynamics and improves mitochondrial function, possibly through the M3R/CaMKK/AMPK pathway, to attenuate ISO-induced cardiac damage in rats. Targeting mitochondrial dynamics may provide a novel therapeutic strategy in IHD.

Keyword :

AMP-activated protein kinase vagal nerve stimulation mitochondrial dynamics mitochondrial function subtype-3 of muscarinic acetylcholine receptor myocardial ischaemia cardioprotection

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GB/T 7714 Xue, Run-Qing , Sun, Lei , Yu, Xiao-Jiang et al. Vagal nerve stimulation improves mitochondrial dynamics via an M-3 receptor/CaMKK/AMPK pathway in isoproterenol-induced myocardial ischaemia [J]. | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE , 2017 , 21 (1) : 58-71 .
MLA Xue, Run-Qing et al. "Vagal nerve stimulation improves mitochondrial dynamics via an M-3 receptor/CaMKK/AMPK pathway in isoproterenol-induced myocardial ischaemia" . | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 21 . 1 (2017) : 58-71 .
APA Xue, Run-Qing , Sun, Lei , Yu, Xiao-Jiang , Li, Dong-Ling , Zang, Wei-Jin . Vagal nerve stimulation improves mitochondrial dynamics via an M-3 receptor/CaMKK/AMPK pathway in isoproterenol-induced myocardial ischaemia . | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE , 2017 , 21 (1) , 58-71 .
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Efficacy of non-cardioplegic radiofrequency ablation Maze-III procedure (RFA Maze-III) for the treatment of atrial fibrillation (AF) during the valve replacement surgery. SCIE Scopus
期刊论文 | 2017 , 28 (7) , 3232-3236 | BIOMEDICAL RESEARCH-INDIA
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Background: The non-cardioplegic surgery has a better myocardial protection compared to cardioplegic surgery. Combination of valve replacement surgery with RFA Maze-III procedure can achieve better clinical efficacy. The goal of this study was to evaluate the efficacy of RAF Maze-III under the non-cardioplegic and mild hypothermic Cardiopulmonary Bypass (CPB) condition for the treatment of chronic Atrial Fibrillation (AF) during the valve replacement surgery. Hypothesis: The non-cardioplegic RFA Maze-III is a safety and efficacy procedure for the treatment of AF during valve replacement surgery. Methods: From 2007 to 2013, 84 consecutive patients with rheumatic heart disease and chronic AF underwent RFA Maze-III and heart valve replacement surgery in our hospital, 46 of which had non-cardioplegic procedure. Continuous electrogram monitoring was performed to observe the cardio-electrical activities of patients during RFA Maze-III and valve replacement surgery. All the patients were follow-up with 24 h Holter and echocardiography in the perioperation and at 12 months after the operation. Results: Sinus rhythm was recovered and maintained perioperatively in 73.7% (28/38) of cases in the cardioplegic group, which was significantly lower than that (91.3%, 42/46) in the non-cardioplegic group. One year after operation, sinus rhythm was maintained in 78.9% (30/38) of cases with cardioplegic surgery, which was significantly lower than that (89.1%, 41/46), in the group with non-cardioplegic surgery. Conclusion: Mild hypothermic non-cardioplegic surgery is feasible, safe and efficient in the treatment of AF by RFA Maze-III. In addition, non-cardioplegic operation simplifies the surgical procedure and makes the process more clearly.

Keyword :

Atrial fibrillation Valve replacement Modified radiofrequency ablation Maze-III procedure (RFA Maze-III) Non-cardioplegic operation

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GB/T 7714 Yan, Yang , Yan, Lu-Qin , Yu, Xiao-Jiang et al. Efficacy of non-cardioplegic radiofrequency ablation Maze-III procedure (RFA Maze-III) for the treatment of atrial fibrillation (AF) during the valve replacement surgery. [J]. | BIOMEDICAL RESEARCH-INDIA , 2017 , 28 (7) : 3232-3236 .
MLA Yan, Yang et al. "Efficacy of non-cardioplegic radiofrequency ablation Maze-III procedure (RFA Maze-III) for the treatment of atrial fibrillation (AF) during the valve replacement surgery." . | BIOMEDICAL RESEARCH-INDIA 28 . 7 (2017) : 3232-3236 .
APA Yan, Yang , Yan, Lu-Qin , Yu, Xiao-Jiang , Zang, Wei-Jin . Efficacy of non-cardioplegic radiofrequency ablation Maze-III procedure (RFA Maze-III) for the treatment of atrial fibrillation (AF) during the valve replacement surgery. . | BIOMEDICAL RESEARCH-INDIA , 2017 , 28 (7) , 3232-3236 .
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MicroRNA-27a/b mediates endothelin-1-induced PPAR gamma reduction and proliferation of pulmonary artery smooth muscle cells SCIE PubMed Scopus
期刊论文 | 2017 , 369 (3) , 527-539 | CELL AND TISSUE RESEARCH | IF: 3.043
WoS CC Cited Count: 3
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Abstract :

The down-regulation of peroxisome proliferator-activated receptor gamma (PPAR gamma) expression has been found to correlate with the proliferation of pulmonary artery smooth muscle cells (PASMC), pulmonary vascular remodeling and pulmonary hypertension, while the molecular mechanisms underlying PPAR gamma reduction in PASMC remain largely unclear. The aim of the current study is to address this issue. Endothelin-1 (ET-1) dose- and time-dependently resulted in PPAR gamma reduction and proliferation of primary cultured rat PASMC, which was accompanied by the activation of nuclear factor-kappaB (NF-kappa B) and subsequent induction of microRNA-27a/b (miR-27a/b) expression. Chromatin immunoprecipitation assay revealed that NF-kappa B directly bound to the promoter regions of miR-27a/b. Luciferase reporter assay identified that miR-27a/b directly regulates the expression of PPAR gamma in PASMC. Further study indicated that the presence of either NF-kappa B inhibitor pyrrolidinedithiocarbamate or prior silencing miR-27a/b with anti-miRNA oligonucleotides suppressed ET-1-induced PPAR gamma reduction and proliferation of PASMC, while overexpression of miR-27a/b reduced PPAR gamma expression and enhanced PASMC proliferation. Taken together, our study demonstrates that ET-1 stimulates miR-27a/b expression by activation of the NF-kappa B pathway, which in turn results in PPAR gamma reduction and contributes to ET-1-induced PASMC proliferation.

Keyword :

Nuclear factor-kappaB miR-27a/b Endothelin-1 Pulmonary hypertension Peroxisome proliferator-activated receptor gamma Pulmonary artery smooth muscle cells

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GB/T 7714 Xie, Xinming , Li, Shaojun , Zhu, Yanting et al. MicroRNA-27a/b mediates endothelin-1-induced PPAR gamma reduction and proliferation of pulmonary artery smooth muscle cells [J]. | CELL AND TISSUE RESEARCH , 2017 , 369 (3) : 527-539 .
MLA Xie, Xinming et al. "MicroRNA-27a/b mediates endothelin-1-induced PPAR gamma reduction and proliferation of pulmonary artery smooth muscle cells" . | CELL AND TISSUE RESEARCH 369 . 3 (2017) : 527-539 .
APA Xie, Xinming , Li, Shaojun , Zhu, Yanting , Liu, Lu , Pan, Yilin , Wang, Jian et al. MicroRNA-27a/b mediates endothelin-1-induced PPAR gamma reduction and proliferation of pulmonary artery smooth muscle cells . | CELL AND TISSUE RESEARCH , 2017 , 369 (3) , 527-539 .
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Erythropoietin ameliorates diabetes-associated cognitive dysfunction in vitro and in vivo SCIE PubMed Scopus
期刊论文 | 2017 , 7 | SCIENTIFIC REPORTS | IF: 4.122
WoS CC Cited Count: 9
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Several studies indicate that erythropoietin (EPO) has remarkable neuroprotective effects in various central nervous system disorders, while little is known about the effects of EPO in diabetes-associated cognitive dysfunction. Therefore, the present study aimed to investigate whether EPO ameliorates diabetes-associated cognitive dysfunction in vivo and in vitro. We investigated the protective effects of EPO on high-glucose (HG)-induced PC12 cell death and oxidative stress. The effects of EPO (300 U/kg administered three times a week for 4 weeks) on diabetes-associated cognitive decline were investigated in diabetic rats. EPO significantly increased cell viability, increased the activity of superoxide dismutase, decreased the production of malondialdehyde and reactive oxygen species, and decreased the apoptosis rate. Additionally, LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, abolished the protective effects of EPO in HG-treated PC12 cells. In diabetic rats, EPO prevented deficits in spatial learning and memory in the Morris water maze test. The results of real-time PCR and Western blotting showed that EPO upregulated EPO receptor, PI3K, and phosphorylated Akt2 relative to unphosphorylated Akt2 (p-Akt2/Akt2) and downregulated glycogen synthase kinase-3 beta (GSK-3 beta). These studies demonstrate that EPO is an effective neuroprotective agent in the context of diabetes-associated cognitive dysfunction and show that this effect involves the PI3K/Akt/GSK-3 beta pathway.

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GB/T 7714 Wang, Meng , Yan, Wenhui , Liu, Yuan et al. Erythropoietin ameliorates diabetes-associated cognitive dysfunction in vitro and in vivo [J]. | SCIENTIFIC REPORTS , 2017 , 7 .
MLA Wang, Meng et al. "Erythropoietin ameliorates diabetes-associated cognitive dysfunction in vitro and in vivo" . | SCIENTIFIC REPORTS 7 (2017) .
APA Wang, Meng , Yan, Wenhui , Liu, Yuan , Hu, Hao , Sun, Qiang , Chen, Xinlin et al. Erythropoietin ameliorates diabetes-associated cognitive dysfunction in vitro and in vivo . | SCIENTIFIC REPORTS , 2017 , 7 .
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Acetylcholine attenuated TNF-alpha-induced intracellular Ca2+ overload by inhibiting the formation of the NCX1-TRPC3-IP3R1 complex in human umbilical vein endothelial cells SCIE PubMed Scopus
期刊论文 | 2017 , 107 , 1-12 | JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | IF: 5.296
WoS CC Cited Count: 2
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The endoplasmic reticulum (ER) forms discrete junctions with the plasma membrane (PM) that play a critical role in the regulation of Ca2+ signaling during cellular bioenergetics, apoptosis and autophagy. We have previously confirmed that acetylcholine can inhibit ER stress and apoptosis after inflammatory injury. However, limited research has focused on the effects of acetylcholine on ER-PM junctions. In this work, we evaluated the structure and function of the supramolecular sodium-calcium exchanger 1 (NCX1)-transient receptor potential canonical 3 (TRPC3)-inositol 1,4,5-trisphosphate receptor 1 (IP3R1) complex, which is involved in regulating Ca2+ homeostasis during inflammatory injury. The width of the ER-PM junctions of human umbilical vein endothelial cells (HUVECs) was measured in nanometres using transmission electron microscopy and a fluorescent probe for Ca2+. Protein-protein interactions were assessed by immunoprecipitation. Ca2+ concentration was measured using a confocal microscope. An siRNA assay was employed to silence specific proteins. Our results demonstrated that the peripheral ER was translocated to PM junction sites when induced by tumour necrosis factor -alpha (TNF-alpha) and that NCX1-TRPC3-IP3R1 complexes formed at these sites. After down-regulating the protein expression of NOC1 or IP3R1, we found that the NCX1-mediated inflow of Ca2+ and the release of intracellular Ca2+ stores were reduced in TNF-alpha-treated cells. We also observed that acetylcholine attenuated the formation of NCX1-TRPO-IP3R1 complexes and maintained calcium homeostasis in cells treated with TNF-alpha. Interestingly, the positive effects of acetylcholine were abolished by the selective M3AChR antagonist darifenacin and by AMPK siRNAs. These results indicate that acetylcholine protects endothelial cells from TNFalpha-induced injury, [Ca2+] overload and ER-PM interactions, which depend on the muscarinic 3 receptor/AMPK pathway, and that acetylcholine may be a new inhibitor for suppressing [Ca2+](cyt), overload. (C) 2017 Elsevier Ltd. All rights reserved.

Keyword :

Muscarinic 3 receptor Endoplasmic reticulum-plasma membrane junctions Acetylcholine Intracellular Ca2+ overload NCX1-TRPC3-IP3R1 complex

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GB/T 7714 Zhao, Ming , Jia, Hang-Huan , Liu, Long-Zhu et al. Acetylcholine attenuated TNF-alpha-induced intracellular Ca2+ overload by inhibiting the formation of the NCX1-TRPC3-IP3R1 complex in human umbilical vein endothelial cells [J]. | JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY , 2017 , 107 : 1-12 .
MLA Zhao, Ming et al. "Acetylcholine attenuated TNF-alpha-induced intracellular Ca2+ overload by inhibiting the formation of the NCX1-TRPC3-IP3R1 complex in human umbilical vein endothelial cells" . | JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 107 (2017) : 1-12 .
APA Zhao, Ming , Jia, Hang-Huan , Liu, Long-Zhu , Bi, Xue-yuan , Xu, Man , Yu, Xiao-Jiang et al. Acetylcholine attenuated TNF-alpha-induced intracellular Ca2+ overload by inhibiting the formation of the NCX1-TRPC3-IP3R1 complex in human umbilical vein endothelial cells . | JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY , 2017 , 107 , 1-12 .
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《临床医学导论》整合课程设计与实践
期刊论文 | 2017 , (5) , 449-453 | 中华医学教育探索杂志
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根据生物-心理-社会医学模式对临床医学生素质培养的要求,以全面提高医学生专业知识、动手能力、人文素质为目标,设计临床医学导论整合课程.通过临床基本职业素养、疾病诊断基本技术、手术相关基本技能、临床医学新进展与技术、临床护理与医护关系、医疗信息管理学六大功能模块,构建临床医学导论整合课程的核心内容.使临床相关基本知识与技能有机整合、临床课程与基础课程紧密衔接、医学与人文并举,为各器官-系统整合课程协同推进奠定基础.

Keyword :

课程整合 临床医学导论 课程设计

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GB/T 7714 和水祥 , 殷燕 , 王云 et al. 《临床医学导论》整合课程设计与实践 [J]. | 中华医学教育探索杂志 , 2017 , (5) : 449-453 .
MLA 和水祥 et al. "《临床医学导论》整合课程设计与实践" . | 中华医学教育探索杂志 5 (2017) : 449-453 .
APA 和水祥 , 殷燕 , 王云 , 张娟 , 李雁 , 习博 et al. 《临床医学导论》整合课程设计与实践 . | 中华医学教育探索杂志 , 2017 , (5) , 449-453 .
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Long-term administration of pyridostigmine attenuates pressure overload-induced cardiac hypertrophy by inhibiting calcineurin signalling SCIE PubMed Scopus
期刊论文 | 2017 , 21 (9) , 2106-2116 | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | IF: 4.302
WoS CC Cited Count: 2 SCOPUS Cited Count: 3
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Abstract :

Cardiac hypertrophy is associated with autonomic imbalance, characterized by enhanced sympathetic activity and withdrawal of parasympathetic control. Increased parasympathetic function improves ventricular performance. However, whether pyridostigmine, a reversible acetylcholinesterase inhibitor, can offset cardiac hypertrophy induced by pressure overload remains unclear. Hence, this study aimed to determine whether pyridostigmine can ameliorate pressure overload-induced cardiac hypertrophy and identify the underlying mechanisms. Rats were subjected to either sham or constriction of abdominal aorta surgery and treated with or without pyridostigmine for 8 weeks. Vagal activity and cardiac function were determined using PowerLab. Cardiac hypertrophy was evaluated using various histological stains. Protein markers for cardiac hypertrophy were quantitated by Western blot and immunoprecipitation. Pressure overload resulted in a marked reduction in vagal discharge and a profound increase in cardiac hypertrophy index and cardiac dysfunction. Pyridostigmine increased the acetylcholine levels by inhibiting acetylcholinesterase in rats with pressure overload. Pyridostigmine significantly attenuated cardiac hypertrophy based on reduction in left ventricular weight/body weight, suppression of the levels of atrial natriuretic peptide, brain natriuretic peptide and -myosin heavy chain, and a reduction in cardiac fibrosis. These effects were accompanied by marked improvement of cardiac function. Additionally, pyridostigmine inhibited the CaN/NFAT3/GATA4 pathway and suppressed Orai1/STIM1 complex formation. In conclusion, pressure overload resulted in cardiac hypertrophy, cardiac dysfunction and a significant reduction in vagal discharge. Pyridostigmine attenuated cardiac hypertrophy and improved cardiac function, which was related to improved cholinergic transmission efficiency (decreased acetylcholinesterase and increased acetylcholine), inhibition of the CaN/NFAT3/GATA4 pathway and suppression of the interaction of Orai1/STIM1.

Keyword :

cardiac hypertrophy acetylcholinesterase calcineurin pyridostigmine

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GB/T 7714 Lu, Yi , Zhao, Ming , Liu, Jin-Jun et al. Long-term administration of pyridostigmine attenuates pressure overload-induced cardiac hypertrophy by inhibiting calcineurin signalling [J]. | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE , 2017 , 21 (9) : 2106-2116 .
MLA Lu, Yi et al. "Long-term administration of pyridostigmine attenuates pressure overload-induced cardiac hypertrophy by inhibiting calcineurin signalling" . | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 21 . 9 (2017) : 2106-2116 .
APA Lu, Yi , Zhao, Ming , Liu, Jin-Jun , He, Xi , Yu, Xiao-Jiang , Liu, Long-Zhu et al. Long-term administration of pyridostigmine attenuates pressure overload-induced cardiac hypertrophy by inhibiting calcineurin signalling . | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE , 2017 , 21 (9) , 2106-2116 .
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Specific alpha 7 nicotinic acetylcholine receptor agonist ameliorates isoproterenol-induced cardiac remodelling in mice through TGF-beta 1/Smad3 pathway SCIE PubMed Scopus
期刊论文 | 2017 , 44 (12) , 1192-1200 | CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY | IF: 2.092
WoS CC Cited Count: 1 SCOPUS Cited Count: 2
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It is well-accepted that inflammation plays an important role in the development of cardiac remodelling and that therapeutic approaches targeting inflammation can inhibit cardiac remodelling. Although a large amount of evidence indicates that activation of alpha 7 nicotinic acetylcholine receptor (alpha 7nAChR) causes an anti-inflammatory effect, the role of alpha 7nAChR in cardiac remodelling and the underlying mechanism have not been established. To investigate the effect of the specific 7nAChR agonist, PNU282987, on cardiac remodelling induced by isoproterenol (ISO 60mg/kg per day) in mice, the cardiomyocyte cross-sectional area (CSA) and collagen volume fraction were evaluated by hematoxylin and eosin (HE) and Masson staining, respectively. Cardiac function and ventricular wall thickness were measured by echocardiography. The protein expressions of collagen I, matrix metalloproteinase 9 (MMP-9), transforming growth factor 1 (TGF-beta 1), and Smad3 were analyzed by Western blot. ISO-induced cardiac hypertrophy, characterized by an increase in the heart weight/body weight ratio, CSA and ventricular wall thickness. Moreover, cardiac fibrosis indices, such as collagen volume fraction, MMP-9 and collagen I protein expression, were also increased by ISO. PNU282987 not only attenuated cardiac hypertrophy but also decreased the cardiac fibrosis induced by ISO. Furthermore, PNU282987 suppressed TGF-beta 1 protein expression and the phosphorylation of Smad3 induced by ISO. In conclusion, PNU282987 ameliorated the cardiac remodelling induced by ISO, which may be related to the TGF-beta 1/Smad3 pathway. These data imply that the alpha 7nAChR may represent a novel therapeutic target for cardiac remodelling in many cardiovascular diseases.

Keyword :

heart remodelling transforming growth factor beta 1 smad3 inflammation alpha 7 nicotinic acetylcholine receptor

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GB/T 7714 Yang, Yong-Hua , Fang, Huan-Le , Zhao, Ming et al. Specific alpha 7 nicotinic acetylcholine receptor agonist ameliorates isoproterenol-induced cardiac remodelling in mice through TGF-beta 1/Smad3 pathway [J]. | CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY , 2017 , 44 (12) : 1192-1200 .
MLA Yang, Yong-Hua et al. "Specific alpha 7 nicotinic acetylcholine receptor agonist ameliorates isoproterenol-induced cardiac remodelling in mice through TGF-beta 1/Smad3 pathway" . | CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY 44 . 12 (2017) : 1192-1200 .
APA Yang, Yong-Hua , Fang, Huan-Le , Zhao, Ming , Wei, Xiang-Lan , Zhang, Ning , Wang, Shun et al. Specific alpha 7 nicotinic acetylcholine receptor agonist ameliorates isoproterenol-induced cardiac remodelling in mice through TGF-beta 1/Smad3 pathway . | CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY , 2017 , 44 (12) , 1192-1200 .
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Choline ameliorates cardiovascular damage by improving vagal activity and inhibiting the inflammatory response in spontaneously hypertensive rats SCIE PubMed Scopus
期刊论文 | 2017 , 7 | SCIENTIFIC REPORTS | IF: 4.122
SCOPUS Cited Count: 1
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Autonomic dysfunction and abnormal immunity lead to systemic inflammatory responses, which result in cardiovascular damage in hypertension. The aim of this report was to investigate the effects of choline on cardiovascular damage in hypertension. Eight-week-old male spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats were intraperitoneally injected with choline or vehicle (8 mg/kg/day). After 8 weeks, choline restored the cardiac function of the SHRs, as evidenced by decreased heart rate, systolic blood pressure, left ventricle systolic pressure, and +/- dp/dt(max) and increased ejection fraction and fractional shortening. Choline also ameliorated the cardiac hypertrophy of the SHRs, as indicated by reduced left ventricle internal dimensions and decreased cardiomyocyte cross-sectional area. Moreover, choline improved mesenteric arterial function and preserved endothelial ultrastructure in the SHRs. Notably, the protective effect of choline may be due to its anti-inflammatory effect. Choline downregulated expression of interleukin (IL)-6 and tumour necrosis factor-a and upregulated IL-10 in the mesenteric arteries of SHRs, possibly because of the inhibition of Toll-like receptor 4. Furthermore, choline restored baroreflex sensitivity and serum acetylcholine level in SHRs, thus indicating that choline improved vagal activity. This study suggests that choline elicits cardiovascular protective effects and may be useful as a potential adjunct therapeutic approach for hypertension.

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GB/T 7714 Liu, Longzhu , Lu, Yi , Bi, Xueyuan et al. Choline ameliorates cardiovascular damage by improving vagal activity and inhibiting the inflammatory response in spontaneously hypertensive rats [J]. | SCIENTIFIC REPORTS , 2017 , 7 .
MLA Liu, Longzhu et al. "Choline ameliorates cardiovascular damage by improving vagal activity and inhibiting the inflammatory response in spontaneously hypertensive rats" . | SCIENTIFIC REPORTS 7 (2017) .
APA Liu, Longzhu , Lu, Yi , Bi, Xueyuan , Xu, Man , Yu, Xiaojiang , Xue, Runqing et al. Choline ameliorates cardiovascular damage by improving vagal activity and inhibiting the inflammatory response in spontaneously hypertensive rats . | SCIENTIFIC REPORTS , 2017 , 7 .
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