检索结果-南通市图书馆

Role of inositol 1,4,5-trisphosphate receptors in α1-adrenergic receptorinduced cardiomyocyte hypertrophy

Acta Pharmacologica Sinica 2006年第7期27卷 895-900页

作者： Da-li LUO~(2,3,5) Jian GAO~2 Xiao-mei LAN~3 Gang WANG~4 Sheng WEI~4 Rui-ping XIAO~4 Qi-de HAN~32 Department of Pharmacology,School of Chemical Biology & Pharmaceutical sciences,Capital university of Medical sciences,beijing 100069,china 3 institute of cardiovascular science at health science center,peking university beijing 100083,china 4 institute of Molecular Medicine and College of Life science,peking university,beijing 100871,china Department of Pharmacology School of Chemical Biology & Pharmaceutical Sciences Capital University of Medical Sciences Beijing China institute of cardiovascular science at health science center Peking University Beijing China institute of Molecular Medicine and College of Life science Peking University Beijing China

Aim:Intracellular Ca2+plays pivotal roles in diverse cellular functions,includinggene transcription that underlies cardiac remodeling during stress ***,the role of inositol 1,4,5-trisphosphate receptors（IP3Rs）in the media-tion of cardiac intracellular Ca2+and hypertrophic growth remains *** with neonatal rat ventricular myocytes suggests that activation of IP3Rsmay be linked to α1adrenergic receptor（α1AR）increased stereotyped Ca2+sparkoccurrence and global Ca2+***,we hypothesized that Ca2+releasethrough IP3Rs was necessary for α1AR-stimulated cardiac ***:We used myoinositol 1,4,5-trisphosphate hexakis（butyryloxymethyl）ester（IP3BM）,a membrane-permeant ester of IP3,to activate IP3Rs directly,and Fluo 4/AM tomeasure intracellular Ca2+***:IP3BM(10μmol·L-1)mimicked theeffects of phenylephrine,a selective agonist of α1AR,in increments in local Ca2+spark release（especially in the perinuclear area）and global Ca2+*** importantly,IP3R inhibitors,2-aminoethoxydiphenyl borateand Xestospongin C,abolished the IP3BM-induced Ca2+responses,and signifi-cantly suppressed α1AR-induced cardiomyocyte hypertrophy assayed by cellsize,[3H]leucine incorporation and atrial natriuretic factor gene expression,dur-ing sustained（48 h）phenylephrine ***:These results,therefore,provide cellular mechanisms that link IP3R signaling to α1AR-stimulatedgene expression and cardiomyocyte hypertrophy.

关键词： inositol 1,4,5-trisphosphate receptors Ca2+sparks α1 adrenergic stimulation cardiac hypertrophy

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Receptor subtype involved in α-adrenergic receptor-mediated Ca2+ signaling in cardiomyocytes

引用

Acta Pharmacologica Sinica 2007年第7期 968-974页

作者： Da-li LUO~(2,3,4),Jian GAO~2,Lin-lin FAN~2,Yu TANG~2,You-yi ZHANG~3,Qi-de HAN~3~2 Department of Pharmacology,School of Chemical Biology and Pharmaceutical sciences,Capital university of Medical sciences,beijing100069,china ~3 institute of cardiovascular science at the health science center,peking university,beijing 100083,china

Aim:The enhancement of intracellular Ca2+signaling in response to α1-adrener-gic receptor （α1-AR） stimulation is an essential signal transduction event in theregulation of cardiac functions,such as cardiac growth,cardiac contraction,andcardiac adaptation to various *** present study was intended todetermine the role（s） of the α1-AR subtype（s） in mediating this ***:We evaluated the effects of subtype-specific agonists and antagonists of the α1-AR on the intracellular Ca2+signaling of neonatal rat ventricular myocytes usinga confocal ***:After being cultured for 48 h,the myocytesexhibited spontaneous local Ca2+release,sparks,and global Ca2+*** of the α1-AR with phenylephrine,a selective agonist of the α1-AR,dose-dependently increased the frequency of Ca2+transients with an EC50valueof 2.3 μmol/*** the α1A-AR subtype with 5-methylurapidil （5-Mu） inhi-bited the stimulatory effect of phenylephrine with an IC50value of 6.7 nmol/***,blockade of the α1B-AR and α1D-AR subtypes with chloroethylclonidineand BMY 7378,respectively,did not affect the phenylephrine ***,thelocal Ca2+spark numbers were also increased by the activation of the α1-AR,andthis effect could be abolished selectively by *** importantly,A61603,anovel selective α1A-AR agonist,mimicked the effects of phenylephrine,but withmore potency (EC50value=6.9 nmol/L) in the potentiation of Ca2+transients,andblockade of the α1A-AR by 5-Mu caused abolishment of its ***:These results indicate that α1-adrenergic stimulation of intracellular Ca2+activityis mediated selectively by the α1A-AR.

关键词： α1-adrenergic receptor subtype cardiomyocyte Ca2+ signaling A61603

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Internalization and distribution of three α1-adrenoceptor subtypes in HEK293A cells before and after agonist stimulation

引用

Acta Pharmacologica Sinica 2007年第3期28卷 359-366页

作者： Shu-yi WANG~2 Yao SONG~2 Ming XU~2 Qi-hua HE~3 Qi-de HAN~2 You-yi ZHANG~(2,4)2 institute of Vascular Medicine,peking university Third Hospital and Key Laboratory of Molecular cardiovascular sciences,Ministry of Education,beijing 100083,china 2 center of Medical Analysis,peking university,health science center,beijing 100083,china institute of Vascular Medicine Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education Beijing China center of Medical Analysis Peking University Health Science Center Beijing China

Aim:To examine the subcellular distribution of the 3 α1-adrenoceptor（α1-AR）subtypes and their internalization and trafficking upon agonist stimulation in hu-man embryonic kidney 293A ***:Confocal real-time imaging,enzymelinked immunosorbent assay（ELISA）and whole cell[3H]-prazosin binding assaywere applied to detect the distribution and localization of the 3 α1B-AR ***:α1A-AR was found both on the cell surface and in the cytoplasm;α1B-AR,however,was predominantly detected on the cell surface,while α1D-AR wasdetected mainly in the intracellular *** stimulation withphenylephrine,localization changes were detected by confocal microscopy forα1A-and α1B-AR, but the localization of α1D-AR were *** promoted a more rapid internalization of α1B-AR than α1A-AR.α1D-ARinternalization was detected only by *** cell[3H]-prazosin bindingassay showed that α1A-AR functional receptors were detected both on the cellsurface and in the cytoplasm;α1B-AR,however,were detected predominantly onthe cell surface,while α1D-AR were detected mainly in intracellular *** stimulation promoted internalization of α1A-and α***:Phenylephrine stimulation induced changes in the localization of the3α1-AR.

关键词： adrenoceptor agonist stimulation confocal image enzyme-linked immunosorbent assay [~3H]-prazosin binding assay internalization subcellular distribution subtype

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Taurine inhibits ischemia/reperfusion-induced compartment syndrome in rabbits

引用

Acta Pharmacologica Sinica 2005年第7期26卷 821-827页

作者： Ji-xian WANG~(2,3) Yan LI~2 Li-ke ZHANG~4 Jing ZHAO~5 Yong-zheng PANG~(2,3) Chao-shu TANG~(3,5) Jing ZHANG~(2,3,6) 1 institute of cardiovascular Disease Research,The First Hospital of peking university,beijing 100034,china 3 Key Laboratory of Molecular cardiovascular science,Ministry of Education,beijing 100083,china 4 Department of Pathophysiology,Capital institute of Medicine,beijing 100054,china 5 Department of Physiology health center of Medical sciences,peking university,beijing 100083,china institute of cardiovascular Disease Research The First Hospital of Peking University Beijing China Key Laboratory of Molecular cardiovascular science Ministry of Education Beijing China Department of Pathophysiology Capital Institute of Medicine Beijing China Department of Physiology Health Center of Medical Sciences Peking University Beijing China

Aim:To investigate effects of taurine on ischemia/reperfusion(I/R)-induced com-partment syndrome in rabbit hind ***:Rabbits underwent femoralartery occlusion after ligation of branches from terminal aorta to femoral *** a 7-h ischemia,reperfusion was established with the use of heparinizedpolyethylene *** received taurine(1 g/kg)or normal saline(control)by iv infusion 10 min before shunt *** reperfusion,anterior com-partment pressure(ACP)was monitored continuously in the left lower *** muscle triphenyltetrazolium chloride(TTC)level,taurine contentand myeloperoxidase activity were *** stress was induced in thein vitro gastrocnemius muscle slices by free radical generating systems(FRGS),and the malondialdehyde content was measured in presence or absence of ***:After 7 h of ischemia,none of the parameters that we measured weredifferent from those before ischemia,except that TTC reduction decreased by80%.In the control group,after 2 h of reperfusion,ACP increased 4.5-fold,andgastrocnemius muscle taurine content was reduced by 33%.In taurine-treatedanimals,at 2 h reperfusion,the mean arterial blood pressure and heart rate wereincreased,by 6% and 10%.ACP decreased by 39%,muscle edema decreased by16%,TTC reduction increased by 150%,and lactate dehydrogenase decreased by36% compared to control *** and muscle taurine content increased by70% and 88%,*** the taurine-treated group,at 2 h repeffusion,plasmamalondialdehyde and conjugated diene content were decreased by 38% and 23%,respectively,and muscle malondialdehyde and conjugated diene content decreasedby 22% and 30%,respectively compared to the control *** 2 h reperfusion,myeloperoxidase activity was increased 3.5-fold in control *** the in vitrostudy,taurine decreased malondialdehyde content in muscle slices incubatedwith hypochlorous acid in a dose-dependent manner,but there was no changewhen incubated

关键词： taurine compartment syndromes reperfu sion injury

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Taurine antagonized oxidative stress injury induced by homocysteine in rat vascular smooth muscle cells

引用

Acta Pharmacologica Sinica 2004年第3期25卷 87-92页

作者： Lin CHANG2,3,Jian-xin XU4,Jing ZHAO5,Yong-zheng PANG2,3,Chao-shu TANG2,3,Yong-fen QI5,6 2institute of cardiovascular Diseases,the FirstHospital,peking university,beijing 100034 3institute of cardiovascular Diseases,peking university,beijing 100083 4instituteof Biophysics,Chinese Academy of sciences,beijing 100101 5Department of Physiology,health science center,peking university,beijing 100083,china institute of cardiovascular Diseases the First Hospital Peking University 北京 100034 institute of Biophysics Chinese Academy of Sciences 北京 100101 Department of Physiology Health Science Center Peking University 北京 100083

AIM: To observe protective effects of taurine on reactive oxygen species generation induced by homocysteine in rat vascular smooth muscle cells (VSMC). METHODS: Rat VSMC was incubated with various concentrations of homocysteine and taurine. The lactate dehydrogenase (LDH) activity which released into culture medium was elevated as an indicator for VSMC injury. The reactive oxygen species (ROS) — hydrogen peroxide (H2O2) and superoxide anion (O2ˉ· )were measured with luminol or lucigenin chemiluminescences method, and the mitochondria Mn-superoxide dismutase (Mn-SOD) and catalase (CAT) were also measured in treated VSMC. RESULTS: LDH leakage from cultured VSMC treated with homocystenie, was increased (P0.05 vs control). In this study, the superoxide anion in VSMC was not detectable by chemiluminent method. In addition, treatment of VSMC with taurine increased mitochondria Mn-SOD and CAT activity in a concentration dependent manner (P<0.05), but homocysteine decreased mitochondria Mn-SOD and CAT activity (P<0.01 vs control). In addition, co-administration of taurine markedly ameliorated homocysteine-induced inhibition of Mn-SOD and CAT activity in VSMC (P<0.01 vs homocysteine alone group). CONCLUSION: Taurine antagonized the effects of homocysteine on ROS generation and anti-oxidant enzyme activities in rat VSMC in vitro.

关键词： homocysteine taurine vascular smooth muscle mitochondria reactive oxygen species

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

p38 MAPK mediates cardiovascular and behavioral responses induced by central IL-1β and footshock in conscious rats

引用

Acta Pharmacologica Sinica 2004年第3期25卷 12-16页

作者： Rui-mao ZHENG,Chang-jiang ZOU,Shi-gong ZHU2 Department of Physiology and Pathophysiology,health science center,peking university,beijing 100083,china Department of Physiology and Pathophysiology Health Science Center Peking University 北京 100083

AIM: To investigate the roles of p38 mitogen-activated protein kinase (p38 MAPK) in the cardiovascular and behavioral responses induced by intracerebral ventricular injection (icv) of interleukin-1β (IL-1β) or footshock. METHODS: We examined the effects of p38 MAPK on mean artery blood pressure (mABP), heart rate (HR), and motor activity (MA) during central administration of IL-1β, or footshock after icv SB203580 (a specific inhibitor of the p38 MAPK) with cardiovascular and Behavior Telemetry System in conscious SD rats. RESULTS: (1) IL-1β (icv) or footshock remarkably rise the mABP, and the maximal changes are (7.8±1.8) and (12.3±3.5) mmHg, respectively, which was abrogated by the pretreatment with p38 inhibitor SB203580 intracerebroventricularly. (2) Compared with icv saline group, the motor activity was significantly decreased in SB203580 group with maximal changes (-7.6±1.1) counts/min after footshock. CONCLUSION: p38 MAPK plays an important role in the pres- sor response induced by central administration of IL-1β or footshock and change of motor activity after footshock in conscious rats.

关键词： mitogen-activated protein kinase p38 interleukin-1 blood pressure motor activity

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats

引用

Acta Pharmacologica Sinica 2006年第3期27卷 299-306页

作者： Sheng-ying WU~(2,6) Chun-shui PAN~3 Bin GENG~3 Jing ZHAO~3 Fang YU~3 Yong-zheng PANG~3 Chao-shu TANG~4 Yong-fen QI~(3,4,5) ~2institute of cardiovascular Disease,peking university First Hospital.beijing 100034 ~3Department of Physiology and Pathophysiology,peking university health science center,beijing 100083,china,~4Key Laboratory of Molecular cardiovascular science,Ministry of Education,beijing 100083,china institute of cardiovascular Disease Peking University First Hospital Beijing China Department of Physiology and Pathophysiology Peking University Health Science Center Beijing China Key Laboratory of Molecular cardiovascular science Ministry of Education Beijing China

Aim:To investigate the role of the endogenous cystathionine γ-synthase(CSE)/hydrogen sulfide(H2S)pathway in vascular calcification in ***:A ratvascular calcification model was established by administration of vitamin D3 plusnicotine(VDN).The amount of CSE and osteopontin(OPN)mRNA was deter-mined by using semi-quantitative reverse-transcription polymerase chain *** calcium content,45Ca2+accumulation and alkaline phosphatase(ALP)activitywere measured.H,S production and CSE activity were ***:yonKossa staining produced strong positive black/brown staining in areas amongthe elastic fibers of the medial layer in the calcified *** calcium content,45Ca2+accumulation and ALP activity in calcified arteries increased by 6.77-,1.42-,and 1.87-fold,respectively,compared with *** expression of the OPNgene was upregulated(P34.8%,40.75% and 63.5% lowerin the low-dosage NariS group than in the VDN group,respectively(P3.9%,37.8 % and 46.2% lower in the aorta in the high-dosage NariS group than in theVDN group,respectively(P<0.01).The expression of the OPN gene ***:The production of H,S,and CSE activity were de-creased and CSE gene expression was downregulated in rats with vascularcalcification.H2S can ameliorate vascular calcification,suggesting that the H2S/CSE pathway plays a regulatory role in the pathogenesis of vascular calcification.

关键词： hydrogen sulfide cystathionine-lyase vascular calcification mRNA

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Sodium hydrosulfide alleviated pulmonary vascular structural remodeling induced by high pulmonary blood flow in rats

引用

Acta Pharmacologica Sinica 2006年第8期27卷 971-980页

作者： Xiao-hui LI~2 Jun-bao DU~(2,6) Ding-fang BU~3 Xiu-ying TANG~4 Chao-shu TANG~5 ~1Department of Pediatrics,peking university First Hospital,Key Laboratory of Molecular cardiovascular Diseases,Ministry of Education ~3 Laboratory center ~4Laboratory of Electron Microscopy,peking university First Hospital,beijing 100034,china ~5Department of Physiology,peking university health science center,beijing 100083,china Department of Pediatrics Peking University First Hospital Key Laboratory of Molecular Cardiovascular Diseases Ministry of Education Beijing China Laboratory center Peking University First Hospital Beijing China Laboratory of Electron Microscopy Peking University First Hospital Beijing China Department of Physiology Peking University Health Science Center Beijing China

Aim:To explore the possible role of endogenous hydrogen sulfide （H2S）,a novelgasotransmitter,in the pathogenesis of pulmonary vascular structural remodeling（PVSR） induced by high pulmonary blood ***:Thirty-two Sprague-Dawley male rats were randomly divided into sham,shunt,sham+NaHS （a H2Sdonor） and shunt+NaHS *** in shunt and shunt+NaHS groups under-went an abdominal aorta-inferior vena cava shunt,and rats in shunt+NaHS andsham+NaHS groups were intraperitoneally injected with *** was inves-tigated using optical microscope and transmission electron *** H2S was evaluated by sulfide-sensitive *** oxide synthase（NOS）,heme oxygenase （HO-1）,proliferative cell nuclear antigen （PCNA） andextracellular signal-regulated kinase （ERK） activation were analyzed by ***:After 11 weeks of shunting,PVSR developed with a decrease inlung tissue H2S production and an increase in nitric oxide （NO）.However,lungtissue carbon monoxide （CO） did not *** the treatment with NaHS for11 weeks,H2S donor ameliorated PVSR and downregulated PCNA expression andERK activation with an increase in lung tissue CO production and HO-1 proteinexpression but a decrease in NO production,NOS activity and eNOS proteinexpression in shunted ***:H2S exerted a regulatory effect on PVSRinduced by high pulmonary blood ***,H2S down-regulated theERK/MAPK signal pathway,inhibited the NO/NOS pathway and enhanced theCO/HO pathway in rats with high pulmonary blood flow.

关键词： hydrogen sulfide pulmonary hypertension structure remodeling nitric oxide/nitric oxide synthase carbon monoxide/heme oxygenase

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Real-time detection of α1A-AR movement stimulated by phenylephrine in single living cells

引用

Acta Pharmacologica Sinica 2007年第6期28卷 796-802页

作者： Ning XU~(2,5),Zhang-yi LIANG~(3,5),Ming XU~2,Ying-hua GUAN~3,Qi-hua HE~4,Qi-de HAN~2,Xin-sheng ZHAO~(3,6),You-yi ZHANG~(2,6)~2 institute of Vascular Medicine,peking university Third Hospital,and Key Laboratory of Molecular cardiovascular sciences,Ministry ofEducation,beijing 100083,china ~3 beijing National Laboratory for Molecular sciences,State Key Laboratory for Structural Chemistry ofUnstable and Stable Species,and Department of Chemical Biology,College of Chemistry and Molecular Engineering,peking university,beijing 100871,china ~4 center of Medical Analysis,peking university,health science center,beijing 100083,china institute of Vascular Medicine Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education Beijing China beijing National Laboratory for Molecular sciences State Key Laboratory for Structural Chemistry of Unstable and Stable Species Department of Chemical Biology College of Chemistry and Molecular Engineering Peking University Beijing China center of Medical Analysis Peking University Health Science Center Beijing China

Aim:To investigate the movement of α1A-adrenergic receptors(α1A-AR) stimu-lated by agonist,phenylephrine （PE）,and the dynamics of receptor movement inreal time in single living cells with millisecond ***:We labeledα1A-AR using the monoclonal,anti-FLAG （a kind of tag） antibody and Cy3-conju-gated goat anti-mouse IgG and recorded the trajectory of their transport processin living HEK293A cells stimulated by agonist,PE,and then analyzed their dy-namic ***:The specific detection of α1A-AR on the surface ofliving HEK293A-α1Acells was achieved.α1A-AR internalize under the stimulationof *** the cells were stimulated with PE for 20 min,apparent colocalizationwas found between α1A-AR and *** 40 min stimulation of PE,trajecto-ries of approximate linear motion in HEK293A-α1Acells were recorded,and theirvelocity was ***:The specific labeling method on the livingcell surface provides a convenient means of real-time detection of the behavior ofsurface *** this method we were able to specifically detect α1A-AR andrecord the behavior of individual particles of receptors with 50 ms exposure time inreal time in single living cells.

关键词： adrenergic receptor trajectory living cell

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

补体相关性肾病诊断和治疗专家共识

引用

中华内科杂志 2024年第3期63卷 258-271页

作者：北京大学医学部肾脏病学系专家组赵明辉不详北京大学第一医院肾内科、北京大学肾脏病研究所北京100034

随着补体系统在各类肾脏疾病中的作用机制逐渐阐明,针对补体活化不同环节的药物相继出现,部分已应用于临床。但补体靶向治疗仍存在诸多问题。北京大学医学系补体相关性肾病诊断和治疗专家共识协作组在国内外肾脏疾病指南/共识的基础上,... 详细信息

随着补体系统在各类肾脏疾病中的作用机制逐渐阐明,针对补体活化不同环节的药物相继出现,部分已应用于临床。但补体靶向治疗仍存在诸多问题。北京大学医学系补体相关性肾病诊断和治疗专家共识协作组在国内外肾脏疾病指南/共识的基础上,结合最新证据制定了本共识,简述了补体相关性肾病的发病机制、诊断思路、补体靶向治疗与特殊致病微生物的疫苗免疫等方面的最新证据和建议,为补体相关性肾病的诊断和治疗提供参考。

关键词：补体相关性肾病诊断治疗补体抑制剂

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：