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ANG相关的网络例句
与 ANG 相关的网络例句 [注:此内容来源于网络,仅供参考]

Methods the rabbit arterial smooth muscle cells were cultured ex vivo, cells of 4-7 generation were divided into groups interfered with ang-(1-7), positive control groupsinterfered with ang-ii(10-6mol/l) and blank control group .cell counting with trypanblau dying and mtt were used to evaluate the growth of cells in different groups and results were compared .

体外培养兔肺动脉平滑肌细胞,鉴定后传代培养,取4~7代细胞,应用不同浓度ang-(1-7)干预,并与血管紧张素-ii(ang-ii,浓度10-6mol/l)、空白组对照。通过台盼蓝染色法细胞计数、四甲基偶氮唑蓝比色法,确定肺动脉平滑肌细胞的生长趋势变化。

The recombinant ANG could obviously promote the proliferation of ECV304 cells. In contrast with the control group, the culture supernatant of pcDNA3. 1-ang transfected group could stimulate the angiogenesis in embryo chorioallantois.

与转染空载体的对照相比,转染pcDNA3.1-ang的细胞培养上清具有促进ECV304细胞增殖的作用,并能显著促进鸡胚尿囊膜血管生长。

ACE inhibitors, which are now widely used for the treatment of hypertension and heart failure, not only block the generation of Ang II from Ang I, but also prevent the degradation of bradykinin.

血管紧张素转换酶抑制剂现今被广泛应用于高血压和心脏病的治疗中,不仅可以抑制Ang I 到Ang II 的转化,同时还可抑制BK 的降解。

Methods: CF were isolated and cultured from Neonatal SD rats.The cells were divided into different groups and treated with Ang-(1-7), TGF-β1, TGF-β1+ Ang-(1-7), and the acceptor inhibiter of TGF-β1 respectively.

分离培养SD仔鼠心脏成纤维细胞,以Ang-(1-7)、TGF-β1、Ang-(1-7)+TGF-β1组、TGF-βⅠ型受体抑制剂等干预,通过WST-1法检测细胞增殖,RT-PCR测定心脏成纤维细胞Smad3、Smad 7mRNA的表达。

RESULTS: Compared with NS control group, the ratio of HW/BW, LVW/BW and the content of hydroxyproline, AngⅡ, MDA and iNOS activity in the left ventricle were significantly increased. The cNOS, SOD, GSH-Px activities and NO content were obriously decreased in the ISO model group. After treatment with PNS, the left ventricular NO content, cNOS, SOD and GSH-Px activities were markedly higher than those in ISO model group. The content of MDA, AngⅡ and iNOS activities and the ratio of HW/BW, LVI were significantly lower than those in ISO model group.

结果:ISO模型组大鼠的HW/BW、LVI、左心室HyP、AngⅡ、MDA含量和诱生型NOS活性显著高于生理盐水对照组,SOD、GSH-Px及结构型NOS活性和NO含量明显比生理盐水对照组低;PNS治疗组左心室心肌组织中NO含量、cNOS、SOD和GSH-Px活性明显高于ISO模型组;MDA和AngⅡ含量及iNOS活性和心脏重量指数比ISO模型组低。

In the bypass path, AngⅠis converted to AngⅡ by ACE of heart and chymase.

而旁路系统是机体最有效和最特异的AngⅡ形成途径。

Plasma Ang Ⅰ and Ang Ⅱ levels, chymase mRNA levels, arteries' PCNA positive percents and the thickness of carotid artery were measured.

通过测定血浆Ang Ⅰ及AngⅡ住水平、糜酶 mRNA表达水平、颈动脉细胞增殖核杭原阳性率及颈动脉各层厚度观察曲尼司特对犬颈动脉损伤后狭窄的作用。

Results As compared to DM control group, levels of GSP, myocardial enzymes and myocardial Ang Ⅱ were much lower in APS group, while levels of insulin, C-peptide and plasma Ang Ⅱ were the same. Levels of expression of collagen Ⅰ and the ratio of collagen Ⅰ/collagen Ⅲ in APS group were lower than those in DM group. APS group showed lower levels of chymase mRNA expression and activity than those in DM control group, while there was no diference in ACE mRNA expression and activity between the two groups.

结果 APS组血糖、糖化血清蛋白、心肌酶谱和心肌Ang Ⅱ水平较DM组显著下降,胰岛素、C肽、血浆AngⅡ水平和DM组无差异;APS组心肌Ⅰ型胶原表达和Ⅰ/Ⅲ型胶原比值较DM组显著下降;APS组chymase mRNA表达和活性均显著低于DM组,ACE基因的表达和活性与DM组无显著性差异。

The CFb in blank control group was added with IMDM containing 10% FBS and those in Ang Ⅱcontrol group with Ang Ⅱ.The CFb in the 3 test groups were induced with Ang II,then added with Tau at dosages of 40,80 and 160 mmol/L respectively. Determine the proliferation of CFb by MTT method, the collagen content by oxyproline kit, the transforming growth factor- TGF-β1 (TGF TGF-β1) content by ELISA, the cell cycle by flow cytometer, the CFb NO content by nitrate reductase method, the iNOS activity by spectrophotometry, and the expression of iNOS protein by IFA.

胰酶消化法分离培养新生大鼠CFb,用Ang Ⅱ诱导促进其增殖,采用MTT法检测细胞增殖;羟脯氨酸试剂盒检测胶原含量;ELISA法测定转化生长因子β1(TGF-β1)蛋白的含量;流式细胞仪检测细胞周期;硝酸还原酶法、分光光度法和免疫荧光法检测CFb NO含量、一氧化氮合酶活性和iNOS蛋白的表达。

Before transfected with AT1, neither AngⅡ nor stretch increased the activation of ERKs. After transfected with AT1, pretreatment with AngⅡ for 8 min or stretch for 10 min activated ERKs obviously.

COS7细胞转染AT1受体以前, AngⅡ和牵张刺激都不能引起细胞内ERKs磷酸化升高;而转染野生型AT1后,AngⅡ和牵张刺激引起细胞内ERKs磷酸化明显升高,各突变体中,Q257A和C289A转染细胞后细胞对牵张刺激的反应受到明显抑制,提示AT1的牵张感受位点在Q257A和C289A。

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