检索结果-南通市图书馆

Cell Research 1999年第2期9卷 155-161页

作者： ZHANG RU GUO LIANG WANG PI LI ZHANG YING XIONG WEN BO ZHANG XING PENG WANG DE LING YIN QING JING (Shanghai Institute of Cell Biology, Chinese Academy of Sciences, 320 Yue Yang Road, Shanghai 200031, China )(Department of Gastroenterology, Shanghai F Shanghai Institute of Cell Biology Chinese Academy of Sciences Shanghai China Department of Gastroenterology Shanghai First People's Hospital Shanghai Medical University Shanghai China

Functional responses to angiotensin ⅱ (AT-Ⅱ) were determined in aortic vascular smooth muscle cells (VSMCs) from experimental cirrhotic rats. Our data showed that AT-Ⅱ-stimulated extracellular acidification rate (ECAR), which was measured by Cytosensor microphysiometry, was significantly reduced in the aortic VSMCs from the cirrhotic rats as compared to those from the control animals. The ability of AT-Ⅱ to promote formation of inositol phosphates, the second messenger produced by the activation of Gq-coupled receptors, was also considerably suppressed in the cirrhotic VSMCs. Furthermore, the maximal p42/44 MAPK phosphorylation stimulated by AT-Ⅱ was significantly reduced in the cirrhotic VSMCs in contrast to that in the normal VSMCs. Taken together, our data clearly demonstrated that the functional responses to AT-Ⅱ was severely suppressed in aortic VSMCs in cirrhosis, indicating the impairment of general Gq-coupled receptor signaling and subsequent biological function in the cirrhotic VSMCs.

关键词： angiotensin ⅱ aortic vascular smooth muscle cells, cirrhosis receptor responses

Relationship between angiotensin-(1-7) and angiotensin ⅱ correlates with hemodynamic changes in human liver cirrhosis

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2009年第20期15卷 2512-2519页

作者： Walkíria Wingester Vilas-Boas Antnio Ribeiro-Oliveira Jr Regina Maria Pereira Renata da Cunha Ribeiro Jerusa Almeida Ana Paula Nadu Ana Cristina Simoes e Silva Robson Augusto Souza dos Santos Laboratory of Hypertension Department of Physiology Biological Sciences institute Federal University of Minas Gerais Av. Antonio Carlos 6627 Belo Horizonte MG 31270-901 Brazil Laboratory of Endocrinology Department of Medicine Faculty of Medicine Federal University of Minas Gerais Av. Alfredo Balena 190 Belo Horizonte MG 30130-100 Brazil Hospitalar Foundation of the State of Minas Gerais FHEMIG Belo Horizonte MG Brazil Department of Pediatrics Faculty of Medicine Federal University of Minas Gerais Av.Alfredo Balena 190 Belo Horizonte MG 30130-100 Brazil

AIM： To measure circulating angiotensins at different stages of human cirrhosis and to further evaluate a possible relationship between renin angiotensin system （RAS） components and hemodynamic changes. METHODS： Patients were allocated into 4 groups： mild-to-moderate liver disease （MLD）, advanced liver disease （ALD）, patients undergoing liver transplantation, and healthy controls. Blood was collected to determine plasma renin activity （PRA）, angiotensin （Ang） Ⅰ, Ang Ⅱ, and Ang-（1-7） levels using radioimmunoassays. During liver transplantation, hemodynamic parameters were determined and blood was simultaneously obtained from the portal vein and radial artery in order to measure RAS components. RESULTS： PRA and angiotensins were elevated in ALD when compared to MLD and controls （P 〈 0.05）. In contrast, Ang Ⅱ was significantly reduced in MLD. Ang-（1-7）/Ang Ⅱ ratios were increased in MLD when compared to controls and ALD. During transplantation, Ang Ⅱ levels were lower and Ang-（1-7）/Ang Ⅱ ratios were higher in the splanchnic circulation than in the peripheral circulation （0.52 ± 0.08 vs 0.38 ±0.04, P 〈 0.02）, whereas the peripheral circulating Ang Ⅱ/Ang Ⅰ ratio was elevated in comparison to splanchnic levels （0.18 ±0.02 vs 0.13 ±0.02, P 〈 0.04）. Ang-（1-7）/ Ang Ⅱ ratios positively correlated with cardiac output （r = 0.66） and negatively correlated with systemic vascular resistance （r = -0.70）. CONCLUSION： Our findings suggest that the relationship between Ang-（1-7） and Ang Ⅱ may play a role in the hemodynamic changes of human cirrhosis.

关键词： Renin-angiotensin system Liver cirrhosis angiotensin-(1-7) angiotensin ⅱ Splanchnic circulation angiotensin converting enzyme 2

Evodiamine Inhibits angiotensin ⅱ-Induced Rat Cardiomyocyte Hypertrophy

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Chinese Journal of Integrative Medicine 2018年第5期24卷 359-365页

作者： HE Na GONG Qi-hai ZHANG Feng ZHANG Jing-yi LIN Shu-xian HOU Hua-hua WU Qin SUN An-sheng Key Laboratory of Basic Pharmacology of Guizhou Departmentof Pharmacology Zunyi Medical College Zunyi GuizhouProvince (563099) China

Objective: To investigate the effects of evodiamine(Evo), a component of Evodiaminedia rutaecarpa(Juss.) Benth, on cardiomyocyte hypertrophy induced by angiotensin ⅱ(Ang Ⅱ) and further explore the potential mechanisms. Methods: Cardiomyocytes from neonatal Sprague Dawley rats were isolated and characterized, and then the cadiomyocyte cultures were randomly divided into control, model(Ang Ⅱ 0.1 μmol/L), and Evo(0.03, 0.3, 3 μmol/L) groups. The cardiomyocyte surface area, protein level, intracellular free calcium([Ca]i) concentration, activity of nitric oxide synthase(NOS) and content of nitric oxide(NO) were measured, respectively. The m RNA expressions of atrial natriuretic factor(ANF), calcineurin(CaN), extracellular signal-regulated kinase-2(ERK-2), and endothelial nitric oxide synthase(e NOS) of cardiomyocytes were analyzed by real-time reverse transcriptionpolymerase chain reaction. The protein expressions of calcineurin catalytic subunit(CnA) and mitogen-activated protein kinase phosphatase-1(MKP-1) were detected by Western blot analysis. Results: Compared with the control group, Ang Ⅱ induced cardiomyocytes hypertrophy, as evidenced by increased cardiomyocyte surface area, protein content, and ANF m RNA expression; increased intracellular free calcium([Ca]i) concentration and expressions of CaN m RNA, CnA protein, and ERK-2 m RNA, but decreased MKP-1 protein expression(P<0.05 or P<0.01). Compared with Ang Ⅱ, Evo(0.3, 3 μmol/L) significantly attenuated Ang Ⅱ-induced cardiomyocyte hypertrophy, decreased the [Ca]i concentration and expressions of CaN m RNA, CnA protein, and ERK-2 m RNA, but increased MKP-1 protein expression(P<0.05 or P<0.01). Most interestingly, Evo increased the NOS activity and NO production, and upregulated the e NOS m RNA expression(P<0.05). Conclusion: Evo significantly attenuated Ang Ⅱ-induced cardiomyocyte hypertrophy, and this effect was partly due to promotion of NO production, reduction of [Ca]i concentration, and inhibition of CaN and

关键词： evodiamine cardiomyocyte hypertrophy angiotensin ⅱ calcineurin extracellular signal regulated kinase-2 nitric oxide

Inhibitory Effects of 2,3,4',5-tetrahydroxystilbene-2-O-β-D-glucoside on angiotensin ⅱ-Induced Proliferation of Vascular Smooth Muscle Cells

在线全文

学校读者我要写书评

暂无评论

Chinese Journal of Integrative Medicine 2015年第3期21卷 204-210页

作者：许晓乐黄燕娟凌丹彦张伟 Department of Pharmacology Nantong University Pharmacy College Shanghai Health Vocational and Technical College

Objective：To investigate the effect of 2,3,4’,5-tetrahydroxystilbene-2-0- p-D-glucoside（TSG）,an active component extracted from the root of Polygonum multiflorum,on angiotensin ⅱ（Ang Ⅱ）-induced proliferation of cultured rat vascular smooth muscle cells（VSMCs） and to identify the potential ***：Cell proliferation and cell cycle were determined by cell counting,5-bromo-2’-deoxyuridine incorporation assay,proliferating cell nuclear antigen protein expression and flow *** of phosphorylated extracellular signal-regulated kinase 1/2（ERK1/2）,mitogenic extracellular kinase 1/2（MEK1/2） and Src in VSMCs were measured by Western *** expression of c-fos,c-jun and c-myc mRNA were measured by reverse transcription polymerase chain reaction（RT-PCR）.Intracellular reactive oxygen species（ROS） was measured by fluorescence ***：TSG significantly inhibited Ang Ⅱ-induced VSMCs proliferation and arrested cells in the G1/S checkpoint（P〈0.05 or P〈0.01）.TSG decreased the levels of phosphorylated ERK1/2,MEK1/2 and Src in VSMCs（P〈0.05 or P〈0.01）.TSG also suppressed c-fos,c-jun and c-myc mRNA expression（P〈0.05 or P〈0.01）.In addition,the intracellular ROS was reduced by TSG（P〈0.01）.Conclusions：TSG inhibited Ang Ⅱ-induced VSMCs *** antiproliferative effect might be associated with down-regulation of intracellular ROS,followed by the suppression of the Src-MEK1/2-ERK1/2 signal pathway,and hence,blocking cell cycle progression.

关键词： 2,3,4’,5-tetrahydroxystilbene-2-O-β-D-glucoside vascular smooth muscle cells proliferation angiotensin ⅱ Chinese medicine Polygonum multiflorum

Influence of connective tissue growth factor antisense oligonucleotide on angiotensin II-induced epithelial mesenchymal transition in HK2 cells

在线全文

学校读者我要写书评

暂无评论

Acta Pharmacologica Sinica 2006年第8期27卷 1029-1036页

作者： Long CHEN Bi-cheng LIU~2 Xiao-liang ZHANG Jian-dong ZHANG Hong LIU Min-xia LI Institute of Nephrology,Zhong Da Hospital,Southeast University School of Medicine,Nanjing 210009,China Institute of Nephrology Zhong Da Hospital Southeast University School of Medicine Nanjing China

Aim:The present study was designed to further investigate the effect of connec-tive tissue growth factor antisense oligonucleotide(CTGF-AS)on angiotensin ⅱ(Ang Ⅱ)-induced tubular cell epithelial mesenchymal transition(EMT)in ***:The human proximal tubular cell line(HK2)was grown in Dulbecco’smodified Eagle’s medium containing 10% heat inactivated fetal calf *** rested in serum-free medium for 24 h,the influence of CTGF-AS(20 μg/mL)on Ang Ⅱ-induced(1×10-7mol/L)CTGF mRNA and the protein expression wereexamined by using reverse transcription-polymerase chain reaction and *** effect of CTGF-AS on Ang Ⅱ-induced cellular ultra-structure was observed using a transmissive electronic *** expres-sion of or-smooth action(α-SMA)was assayed by *** allexperiments,the control group was treated with scrambled ***:It was shown that Ang Ⅱ significantly induced the increasing expressionof CTGF mRNA and protein(P<0.01,respectively),which were significantly abol-ished by treatment with *** stimulating cells with Ang Ⅱ,the cellularultrastructure showed mesenchymal *** effects were partially inhib-ited by *** Ⅱ significantly resulted in the expression of α-SMA in timedependent manner,which was markedly attenuated by the treatment with CTGF-AS(P<0.01,respectively).In contrast,no similar effects were observed in thecontrol group treated with scrambled ***:Ang Ⅱ-in-duced EMT in human proximal tubular epithelial cells(PTC)can be attenuated bytreatment with *** data provides further evidence that CTGF might beinvolved in Ang Ⅱ-induced EMT in PTC.

关键词： connective tissue growth factor angiotensin ⅱ epithelial mesenchymal transition proximal kidney tubules humans

All-trans retinoic acid inhibited angiotensin ⅱ-induced increase in cell growth and collagen secretion of neonatal cardiac fibroblasts

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Acta Pharmacologica Sinica 2006年第4期27卷 423-429页

作者： Yan HE~2 Ying HUANG~2 Li ZHOU~2 Li-min LU~2 Yi-chun ZHU~2 Tai YAO~(2,3,4) ~2Department of Physiology and Pathophysiology,and ~3State Key Laboratory for Medical Neurobiology.Fudan University Shanghai Medical College.Shanghai 200032.China Department of Physiology and Pathophysiology Fudan University Shanghai Medical College Shanghai China State Key Laboratory for Medical Neurobiology Fudan University Shanghai Medical College Shanghai China

Aim:To determine whether all-trans retinoic acid(atRA)acts to modulate angio-tensin Ⅱ(Ang Ⅱ)-induced cardiac fibroblast cell growth and collagen ***:Cultured neonatal rat cardiac fibroblasts(CF)were used in the experiment.A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT)assay wasused to detect cell growth of the CF;and immunocytochemistry and Westernblotting were used to measure the production and secretion of collagen and theexpression of transforming growth factor-β1(TGF-β1)by the ***:atRA(1×10-7to 1×10-5mol/L)inhibited the Ang Ⅱ-induced increase in cell growth of CF(P<0.05).Ang Ⅱ stimulated the secretion of collagen types Ⅰ and Ⅲ by the *** effect was blocked by AT1receptor antagonist losartan(1×10-6mol/L),butnot by AT2receptor antagonist PD 123319 (up to 1×10-6mol/L).Exposure of CF toatRA(1×10-5mol/L)attenuated the Ang Ⅱ-induced increase in the secretion ofcollagen types Ⅰ and Ⅲ(P<0.05).atRA (1×10-5mol/L)also blocked the Ang Ⅱ-induced increase in the expression of TGF-β***:atRA inhibits the AngⅡ-induced increase in cell growth and collagen secretion of neonatal rat *** of atRA is possibly mediated by lowering the TGF-β*** observa-tions support the notion that atRA is a potential candidate for the prevention andtherapy of cardiac remodeling.

关键词： cardiac fibroblast angiotensin ⅱ all-trans retinoic acid collagen secretion transforming growth factor-β1

Rapamycin Treatment Attenuates angiotensin ⅱ-induced Abdominal Aortic Aneurysm Formation via VSMC Phenotypic Modulation and Down-regulation of ERK1/2 Activity

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Journal of Huazhong University of Science and Technology(Medical Sciences) 2018年第1期38卷 93-100页

作者： Fei-fei LI Xiao-ke SHANG Xin-ling DU Shu CHEN Department of Cardiovascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China

The aim of the present study is to address the effect of rapamycin on abdominal aortic aneurysm（AAA） and the potential mechanisms. A clinically relevant AAA model was induced in apolipoprotein E-deficient（ApoE-/-） mice, in which miniosmotic pump was implanted subcutaneously to deliver angiotensin ⅱ（Ang Ⅱ） for 14 days. Male ApoE-/-mice were randomly divided into 3 groups： saline infusion, Ang Ⅱ infusion, and Ang Ⅱ infusion plus intraperitoneal injection of rapamycin. The diameter of the supra-renal abdominal aorta was measured by ultrasonography at the end of the infusion. Then aortic tissue was excised and examined by Western blotting and histoimmunochemistry. Ang Ⅱ with or without rapamycin treatment was applied to the cultured vascular smooth muscle cells（VSMCs） in vitro. The results revealed that rapamycin treatment significantly attenuated the incidence of Ang Ⅱinduced-AAA in ApoE-/-mice. Histologic analysis showed that rapamycin treatment decreased disarray of elastin fibers and VSMCs hyperplasia in the medial layer. Immunochemistry staining and Western blotting documented the increased phospho-ERKl/2 and ERK1/2 expression in aortic walls in Ang Ⅱ induced-AAA,as well as in human lesions. Whereas in the rapamycintreated group, decreased phospho-ERK1/2 expression level was detected. Moreover, rapamycin reversed Ang Ⅱ-induced VSMCs phenotypic change both in vivo and in vitro. Based on those results, we confirmed that rapamycin therapy suppressed Ang Ⅱ-induced AAA formation in mice, partially via VSMCs phenotypic modulation and down-regulation of ERK1/2 activity.

关键词： rapamycin abdominal aortic aneurysm angiotensin ⅱ extracellular signal-regulated kinase vascular smooth muscle cells phenotypic modulation

Valsartan Inhibits angiotensin ⅱ-induced Proliferation of Vascular Smooth Muscle Cells via Regulating the Expression of Mitofusin 2

在线全文

学校读者我要写书评

暂无评论

Journal of Huazhong University of Science and Technology(Medical Sciences) 2012年第1期32卷 31-35页

作者：廖华龚俊荣张文娟郭小梅 Department of Cardiology Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology Department of Cardiology the Central Hospital of Wuhan

angiotensin ⅱ (ANGⅡ) plays an important role in the pathogenesis of atherosclerosis by inducing proliferation of vascular smooth muscle cells (VSMCs).In our study,we observed the effects of valsartan on proliferation of cultured VSMCs treated with or without ANGⅡ by cell counting and methyl thiazolyl tetrazolium (MTT) assay,and detected the expression of mitofusin 2 (Mfn2),a newly discovered cell proliferation inhibitor and a related cell proliferation signaling pathway pro-tein by Western ***Ⅱ at a concentration of 10-6 mol/L significantly stimulated VSMCs proliferation,down-regulated the expression of Mfn2 and upregulated the expression of Raf and ERK1/*** inhibited such effects of ANGⅡ at concentrations of 10-5 and 10-6 mol/L,but not at 10-7 mol/*** had no significant effect on the proliferation of untreated *** results suggest that valsartan inhibits ANGⅡ-induced proliferation of VSMCs in vitro via Mfn2-Ras-Raf-ERK/MAPK signaling pathway.

关键词： valsartan angiotensin ⅱ vascular smooth muscle cells proliferation mitofusin 2

Effect of Sodium Tanshinone ⅡA Sulfonate on Phosphorylation of Extracellular Signal-regulated Kinasel/2 in angiotensin ⅱ-induced Hypertrophy of Myocardial Cells

在线全文

学校读者我要写书评

暂无评论

Chinese Journal of Integrative Medicine 2008年第2期14卷 123-127页

作者：李树生冯俊郑智梁黔生 Department of Emergency Internal Medicine Tongji Hospital Huazhong University of Science and Technology

Objective： To observe the effects of sodium tanshinone ⅡA sulfonate （STS） on angiotensin ⅱ （Ang Ⅱ）-induced hypertrophy of myocardial cells through the expression of phosphorylated extracellular signal-regulated kinase （p-ERK1/2）. Methods： In the primary culture of neonatal rat myocardial cells, the total protein content in myocardial cells was determined by coomassie brilliant blue and the protein synthesis rate was measured by [3H]-Leucine incorporation as indexes for hypertrophy of myocardial cells. The expression of p-ERK1/2 was determined using Western blot and immunofluorescence labeling. Results：（1） The total protein and protein synthesis rate increased significantly in contrast to the control group after the myocardial cells were stimulated by Ang Ⅱ （1 μ mol/L） for 24 h; STS markedly inhibited the increment of the total protein level induced by Ang Ⅱ and the syntheses of protein. （2） After pretreatment of myocardial cells with Ang Ⅱ （1 μmol/L） for 5 min, the p-ERK1/2 protein expression was increased, with the most obvious effect shown at about 10 min; pretreatment of myocardial cells with STS at different doses （2, 10, 50μmol/L） for 30 min resulted in obvious inhibition of the expression of p-ERK1/2 stimulated by Ang Ⅱ in a dose-dependent manner. （3） After the myocardial cells were stimulated by AngⅡ （1 μ mol/L）, the immunofluorescence of ERK1/2 rapidly appeared in the nucleus. The activation and translocation process of ERK1/2 induced by Ang Ⅱ was blocked distinctly by STS. （Conclusion： STS inhibited the myocardial cell hypertrophy induced by Ang Ⅱ, and the mechanism may be associated with the inhibition of p-ERK1/2 expression.

关键词： sodium tanshinone Ⅱ A sulfonate angiotensin ⅱ myocardial cell hypertrophy extracellular signal-regulated kinase

Association of Polymorphisms in angiotensin-converting Enzyme and Type 1 angiotensin ⅱ Receptor Genes with Coronary Heart Disease and the Severity of Coronary Artery Stenosis

在线全文

学校读者我要写书评

暂无评论

Journal of Huazhong University of Science and Technology(Medical Sciences) 2007年第6期27卷 660-663页

作者：邱春光韩战营卢文杰张存泰 Department of Cardiology Tongji Hospital Huazhong University of Science and Technology

To explore the relation of angiotensin-converting enzyme （ACE） and angiotensin ⅱ type 1 receptor （AT1R） gene polymorphism with coronary heart disease （CHD） and the severity of coronary artery stenosis, 130 CHD patients who underwent coronary angiography were examined for the number of affected coronary vessels （≥75% stenosis） and coronary Jeopardy score. The insertion/deletion of ACE gene polymorphism and AT1R gene polymorphism （an A→C transversion at nucleotide position 1166） were detected by using polymerase chain reaction （PCR） and restriction fragment length polymorphism （RFLP） in CHD patients and 90 healthy serving as controls. The resuits showed that DD genotype and of ACE were more frequent in CHD patients than that in control group （38.5% vs 14.4%, P〈0.001）. The frequency of the ATIR A/C genotypes did not differ between the patients and the controls （10% vs 13.1%, P〉0.05）. The relative risk associated with the ACE-DD was increased by AT1R-AC genotype. Neither the number of affected coronary vessels nor the coronary score differed among the ACE I/D genotypes （P〉0.05）. But the number of affected coronary vessels and the coronary score were significantly greater in the patients with the AT1R-AC genotype than in those with the AA genotype （P〈0.05）. In conclusion, DD genotype may be risk factor for CHD and MI in Chinese people, and is not responsible for the development of the coronary artery stenosis. The AT1R-C allele may increase the relative risk associated with the ACE-DD genotype, and may be involved in the development of the stenosis of coronary artery.

关键词： angiotensin Ⅰ-converting enzyme angiotensin ⅱ receptor gene polymorphism coronary angiography