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urotensin Ⅱ receptor antagonist reduces hepatic resistance and portal pressure through enhanced eNOS-dependent HSC vasodilatation in CCI4-induced cirrhotic rats

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Frontiers of Medicine 2019年第3期13卷 398-408页

作者： Ruoxi Zhang Jing Chen Diangang Liu Yu Wang Department of General Surgery Xuanwu HospitalCapital Medical UniversityBeijing 100053China Department of Gastroenterology the Second Affiliated Hospital of Harbin Medical UniversityHarbin 150010China Department of General Surgery Beijing Friendship HospitalCapital Medical UniversityBeijing 100050China

Increased serum urotensin Ⅱ(UⅡ) levels in human cirrhotic populations have been recently shown,but the long-term effects of UⅡ receptor antagonist on the cirrhosis have not been *** investigate the therapeutic effects of urotensin Ⅱ receptor (UT) antagonist palosuran on rats with carbon tetrachloride (CCI4)- induced cirrhosis,the hepatic and systemic hemodynamics,liver fibrosis,the metalloproteinase-13 (MMP-13)/ tissue inhibitor of metalloproteinase-1 (TIMP-1) ratio,hepatic Rho-kinase activity,and the endothelial nitric oxide synthase (eNOS) activity are measured in CCI4-cirrhotic rats treated with palosuran or vehicle for 4 *** hepatic stellate cells (HSCs) are used to investigate the changes in UⅡ/UT expression and the in vitro effect of *** with the vehicle-treated cirrhotic rats,treatment with palosuran can reduce the portal pressure (PP),decrease the risk of liver fibrosis and the level of a smooth muscle actin,collagen-l (COL-I),and transforming growth factor β ***,treatment with palosuran can increase MMP-13/TIMP-1,pvasodilator- stimulated phosphoprotein (p-VASP),and p-eNOS ***,in vitro UⅡ/UT mRNA expression increases during HSC ***-13/TIMP-1,COL-I,and p-VASP are inhibited after palosuran treatment Our data indicate that long-term administration of palosuran can decrease PP in cirrhosis,which results from decreased hepatic fibrosis and enhanced eNOS-dependent HSC vasodilatation.

关键词： portal hypertension cirriiosis urotensin Ⅱ palosuran hepatic stellate cell

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urotensin Ⅱ increases endothelin production by vascular smooth muscle cells in rats

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Chinese Science Bulletin 2002年第12期47卷 1007-1010页

作者： Ql Yongfen, BU Dingfang, YANG Jun, ZHANG Zhaokang, NIU Dadi, SHI Yanrong, ZHANG Zhenghao, TANG Chaoshu & DU JunbaoInstitute of Cardiovascular Diseases, The First Hospital of Peking University, Beijing 100083, China Department of Physiology, Health Science Institute of Cardiovascular Diseases First Hospital of Peking University Beijing 100083 China

The aim of this study was to observe the effects of urotensin Ⅱ (UII) on production of endothelin (ET) in rat aortic vascular smooth muscle cells (VSMC). Cultured VSMCs incubated with various concentrations of UII were used to measure the YSMC 3H-TdR incorporation, the amount of ET mRNA and ET production in VSMCs. In this work we found that UII (10-10-10-8 mol/L) promoted VSMC 3H-TdR incorporation (47%-83%, P<0.01) and increased the amount of ET mRNA by 17.1% (P < 0.05) to 112.8% (P < 0.01), respectively, in a concentration dependent manner compared with control. After 4 and 8 h incubation, 10-10-10-8 mol/L of UII elevated the ET synthesis and release in a concentration dependent manner. After 4 h incubation, the content of ET in medium was 4.9, 5.36 and 7.12 pg/mL (P < 0.01). After 8 h incubation, the ET content released from VSMCs was 12.6, 12.07 and 17.17 pg/mL (P < 0.01). In addition, it was found that BQ123, a specific ETA receptor antagonist, obviously decreased the VSMC DNA synthesis induced by

关键词： urotensin II endothelin mRNA peptide/interaction.

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Adrenomedullin inhibits the endothelin production induced by urotensin Ⅱ in rat vascular smooth muscle cells

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Chinese Science Bulletin 2002年第17期47卷 1457-1461页

作者： Ql Yongfen BU Dingfang YANG Jun ZHANG Zhaokang SHI Yanrong PANG Yongzheng TANG Chaoshu Institute of Cardiovascular Diseases The First HospitalPeking UniversityBeijing 100034China Phoenix Pharmaceutical Inc.2438 Wyandotte Street Montain View Department of Physiology Healh Science CenterPeking UniversityBeijing 100083China

The aim of this study was to observe the effects of adrenomedullin (ADM) on endothelin (ET) production induced by urotensin Ⅱ (UⅡ) in rat vascular smooth muscle cells (VSMCs). Cultured VSMCs which were incubated with UⅡ (10-8 mol/L) and with various concentrations of ADM were used to measure the VSMCs 3H-TdR incorporation, the activity of extracellular signal-regulated kinase (ERK), the amount of ET mRNA and ET production in VSMCs. In this work we found that incubation with UⅡ (10-8 mol/L) increased obviously the amount of ET mRNA in VSMCs and ET production in medium, however, co-incubation with ADM (10-10-10-8 mol/L) and UⅡ(10-8 mol/L) reduced the amount of ET mRNA by 15%, 24% and 45% (P< 0.01) respectively, compared with UⅡ alone. The content of ET in medium was 14.13, 11.38 and 11.00 pg/mL. ADM alone (10-8 mol/L) had no effect on ET production in VSMCs. UⅡ (10-8 mol/L) promoted the 3H-TdR incorporation and activity of ERK in VSMCs. ADM inhibited VSMCs 3H-TdR incorporation and activation of

关键词： adrenomedullin urotensin II endothelin mRNA pep-tide/interaction.

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Decreased plasma urotensin Ⅱ levels inversely correlate with extent and severity of coronary artery disease

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Journal of Geriatric Cardiology 2007年第2期4卷 105-110页

作者： V. Borlongan Christine E. Stahl Department of Neurology Medical College of Georgia Augusta GA 30912 USA Department of Internal Medicine Dwight D. Eisenhower Army Medical Center Fort Gordon GA 30909 USA

Objective To determine the plasma urolensin Ⅱ(UII) levels in various types of coronary heart disease and to clarify how the plasma UII levels correlate with the clinical presentation, extent and severity of coronary artery atherosclerosis (CAD). Methods: One hundred and three aged patients undergoing elective diagnostic coronary angiography for proven or clinical suspected coronary heart disease were enrolled in this study. The extent and severity of coronary artery disease were evaluated by vessel score and Gensini score, respectively. Plasma UII levels were measured by radioimmunoassay. Results: The plasma UII levels in the patients with modest to severe coronary stenosis (3.03±0.34 pg/ml, 1.83±0.67 pg/ml) were significantly lower than that in subjects with normal coronary artery (4.80±1.11 pg/ml, P<0.001). The plasma UII levels in patients with coronary heart disease were also significantly lower than that in patients with insignificant coronary stenosis (P < 0. 001). Compared to patients with stable angina pectoris, plasma UII levels in patients with acute coronary syndrome were significantly decreased (1.89±0.51 pg/ml vs 2.42±0.77 pg/ml, P < 0.001). Plasma UII levels were found to be negatively correlated with the severity of coronary artery stenosis (r = -0.488, P<0.001), as well as the vessel score (r = -0.408, P<0.05) in the patients with CAD. Conclusion: Significant inverse correlations exist between the plasma UII levels, and the extent and severity of coronary artery stenosis. These findings suggest that plasma UII contribute to the development and progression of coronary artery stenosis, and may be a novel marker to predict clinical types, as well as the extent and severity of coronary artery disease in the patients.

关键词： urotensin Ⅱ Coronary artery atherosclerosis Coronary heart disease

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Association of urotensin Ⅱ with angiographic severity of coronary artery disease

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Journal of Geriatric Cardiology 2007年第4期4卷 229-232页

作者： Lifang Zhang Yuannan Ke Yong Wang Xianlun Li Li Chen Chinese Academy of Medical Sciences & Peking Union Medical College Department of Cardiology China-Japan Friendship Hospital Beijing 100029 China Chinese Academy of Medical Sciences & Peking Union Medical College Department of Cardiology China-Japan Friendship Hospital Beijing 100029 China Chinese Academy of Medical Sciences & Peking Union Medical College Department of Cardiology China-Japan Friendship Hospital Beijing 100029 China Chinese Academy of Medical Sciences & Peking Union Medical College Department of Cardiology China-Japan Friendship Hospital Beijing 100029 China Chinese Academy of Medical Sciences & Peking Union Medical College Department of Cardiology China-Japan Friendship Hospital Beijing 100029 China

Objective The goal of this study was to examine the association between urotensin Ⅱ (U Ⅱ) concentration and the severity of coronary artery disease (CAD). Methods We studied U Ⅱ concentrations in 100 patients with known or suspected CAD referred for cardiac catheterization. Based on coronary angiograms, subjects were classified as having no or mild CAD (stenosis 0.05), but higher in the severe group (score =9) than in the normal or nearly normal group (score<3)(2.50±1.62pmol/L vs 1.61±1.05pmol/L, P=0.03). UⅡ concentration had no relationship with other known risk factors, but it correlated with CAD severity (r=0.213, P=0.034). In multiple regression analysis, U Ⅱ is one of the determinants of the severity of CAD, other than age, abnormal glucose, hypertension and gender. Conclusios U Ⅱ is elevated in severe CAD and there is a significant relationship between U Ⅱ concentration and CAD severity. (J Geriatr Cardiol 2007;4:229-232.)

关键词： arteriosclerosis urotensin Ⅱ coronary artery disease

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urotensin Ⅱ在急性肝衰竭小鼠肝组织中的表达及损伤作用

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世界华人消化杂志 2012年第18期20卷 1616-1622页

作者：刘亮明梁冬雨张芳芳于芳苹赵亮叶长根上海交通大学附属第一人民医院松江分院上海市201600

目的:探讨urotensin Ⅱ(UⅡ)在急性肝衰竭(acute liver failure,ALF)小鼠肝组织中的表达及损伤作用.方法:♂Balb/c小鼠随机分成4组(每组6只):正常对照组(A组)、预处理对照组(B组)、模型组(C组)和预处理模型组(D组).模型动物以脂多糖(lip... 详细信息

目的:探讨urotensin Ⅱ(UⅡ)在急性肝衰竭(acute liver failure,ALF)小鼠肝组织中的表达及损伤作用.方法:♂Balb/c小鼠随机分成4组(每组6只):正常对照组(A组)、预处理对照组(B组)、模型组(C组)和预处理模型组(D组).模型动物以脂多糖(lipopolysaccharide,LPS)/D-半乳糖胺(D-galactosamine,D-GalN)腹腔注射,预处理动物在造模前30min,用UⅡ受体拮抗剂Urantide0.6mg/kg尾静脉注射.LPS/D-GalN攻击12h后,采集血清和肝组织标本,并观察24h小鼠存活情况;采用Reitman-Frankel法检测血清丙氨酸氨基转移酶(alanine aminotransferase,ALT)和天冬氨酸氨基转移酶(aspartate amino-transferase,AST)活性水平;采用HE染色显微镜观察肝组织损伤程度;RT-PCR法检测UⅡ及其受体UTmRNA的表达;ELISA法检测血清UⅡ多肽分泌水平;免疫组织化学方法检测肝组织UⅡ多肽及其UT受体蛋白质表达.结果:C组小鼠死亡率为66.7%,A、B和D组所有动物均存活;LPS/D-GalN攻击引起C和D组小鼠血清ALT和AST水平显著升高(P<0.01),而D组较C组显著降低(2271.09U/L±102.24U/Lvs1160.67U/L±258.32U/L,1569.42U/L±204.04U/Lvs1030.31U/L±108.09U/L,P<0.01);C组小鼠肝组织结构破坏明显,见大片出血性坏死及炎症表现,D组肝组织结构保持完整,仅有局灶性出血坏死,炎症明显减轻;C和D组小鼠血清UⅡ多肽水平较A和B组高(P<0.01),但D组较C组明显降低(3.73g/L±0.52g/Lvs1.90g/L±0.27g/L,P<0.01);LPS/D-GalN诱导了C和D组小鼠肝组织UⅡ和UT的mRNA及蛋白质高水平表达,而D组的表达水平较C组显著降低(P<0.01).结论:LPS/D-GalN可诱导ALF小鼠肝组织表达和分泌UⅡ,并促进肝组织UT受体的表达;UⅡ的表达与分泌可能存在正反馈调控机制;UⅡ/UT受体介导了LPS/D-GalN诱导的ALF的发生.

关键词：急性肝衰竭 urotensin Ⅱ UT受体 Urantide

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蛋白激酶Cξ亚型基因及urotensinⅡ基因中各有一个单核苷酸位点与中国北方汉族人群2型糖尿病相关

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中国医学科学院学报 2002年第3期24卷 223-227页

作者：孙红霞杜玮南左瑾吴国栋史贵彬沈岩强伯勤姚志建杭建梅王姮黄薇陈竺方福德中国医学科学院中国协和医科大学基础医学研究所医学分子生物学国家重点实验室北京100005

目的采用单核苷酸多态性(singlenucleotidepolymorphism,SNP)标记,在以往中国北方汉族人群2型糖尿病相关基因定位区域(1p36.33-p36.23)内寻找疾病易感基因位点。方法通过生物信息学方法在公共SNP数据库中查找定位区域内10个候选基因中... 详细信息

目的采用单核苷酸多态性(singlenucleotidepolymorphism,SNP)标记,在以往中国北方汉族人群2型糖尿病相关基因定位区域(1p36.33-p36.23)内寻找疾病易感基因位点。方法通过生物信息学方法在公共SNP数据库中查找定位区域内10个候选基因中的23个SNP位点,用单碱基延伸反应(singlebaseextension,SBE)法对北方汉族人群散发2型糖尿病患者(192例)及对照组(172例)进行分型及病例-对照关联分析。结果23个SNP位点中有8个为中国北方人群常见SNP位点;对病例组和对照组分型分析显示,位于蛋白激酶Cξ亚型(PRKCZ)基因中的一个位点(rs436045)及urotensinⅡ(UTS2)基因中的一个位点(rs228648),其等位基因频率在两组的差异具有统计学意义(P<0.05)。结论上述两个SNP位点可能和中国北方汉族人群2型糖尿病相关,以上结果为进一步研究上述两个位点所在的基因与2型糖尿病的关系提供了理论依据。

关键词：慢白激酶Cζ亚型基因 urotensin Ⅱ基因中国北方汉族人群单核苷酸多态性标记 2型糖尿病病例-对照关联分析

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urotensin Ⅱ对心力衰竭大鼠心功能的影响及其作用机制探讨

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中西医结合心脑血管病杂志 2008年第1期6卷 38-40页

作者：李晨娟韩清华山西医科大学第一医院

目的观察不同浓度urotensinⅡ(UⅡ)对心力衰竭大鼠心功能的影响,及特异性的PKA抑制剂(KT5720)对UⅡ作用于心力衰竭大鼠心脏效应的影响。方法在Langendorff离体心脏灌注模型上,观察给予不同浓度的UⅡ后大鼠心功能的变化(UⅡ组);KT5720加... 详细信息

目的观察不同浓度urotensinⅡ(UⅡ)对心力衰竭大鼠心功能的影响,及特异性的PKA抑制剂(KT5720)对UⅡ作用于心力衰竭大鼠心脏效应的影响。方法在Langendorff离体心脏灌注模型上,观察给予不同浓度的UⅡ后大鼠心功能的变化(UⅡ组);KT5720加UⅡ处理组,在灌流KT5720基础上给予UⅡ(>IC50),观察大鼠心功能指标的变化;KT5720对照组,给予KT5720后观察大鼠心功能的变化。结果UⅡ组给予不同浓度的UⅡ灌注后,大鼠心功能指标灌注压、LVEDP升高,其余指标呈明显下降趋势,KT5720加UⅡ处理组,+dp/dtmax降低了3.27%,-dp/dtmax降低3.15%,与UⅡ组的±dp/dtmax抑制率组间比较,有统计学意义(P<0.01);KT5720对照组,给予KT5720后,+dp/dtmax降低2.84%,-dp/dtmax降低2.96%,与KT5720加UⅡ处理组比较无统计学意义。结论UⅡ对大鼠心脏功能呈剂量依赖性抑制,KT5720可以阻断UⅡ对大鼠心脏的抑制作用,UⅡ对心功能的抑制作用可能是通过PKA途径起作用。

关键词： urotensin Ⅱ KT5720 心功能心力衰竭大鼠

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urotensinⅡ对大鼠心功能的影响及其作用机制的探讨

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中国药理学通报 2008年第4期24卷 560-560页

作者：李晨娟韩清华山西医科大学第一医院心内科山西太原030001

尾加压素Ⅱ（urotensinⅡ，UⅡ）是迄今为止发现的最强的缩血管物质，主要分布于心血管系统及神经系统。本实验观察UⅡ对大鼠心功能的影响，探讨其可能的信号转导机制。

关键词： urotensin Ⅱ 作用机制 KT5720 离体心脏心功能

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urotensin Ⅱ诱导HepG2细胞胰岛素抵抗模型的建立及机制探讨

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中国病理生理杂志 2015年第10期 1875-1875页

作者：李莹莹禹晓童王学江首都医科大学

目的:采用urotensin Ⅱ(UⅡ)体外诱导法建立HepG 2细胞胰岛素抵抗模型,并探讨其机制。方法:采用含不同UⅡ浓度的DMEM培养基培养HepG 2细胞,最后半小时与1×10-7mol/L insulin共孵育,葡萄糖-己糖激酶法检测不同时点培养基中葡萄糖含量,以... 详细信息

目的:采用urotensin Ⅱ(UⅡ)体外诱导法建立HepG 2细胞胰岛素抵抗模型,并探讨其机制。方法:采用含不同UⅡ浓度的DMEM培养基培养HepG 2细胞,最后半小时与1×10-7mol/L insulin共孵育,葡萄糖-己糖激酶法检测不同时点培养基中葡萄糖含量,以HepG 2细胞蛋白进行定量,确定胰岛素抵抗最佳作用浓度及时间;多功能酶标仪检测UⅡ诱导hepG 2细胞内活性

关键词：胰岛素抵抗 HepG2 urotensin 细胞

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