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肝细胞游离钙
相关语句
  cellular free calcium
     PREVENTIVE EFFECT OF GANFUKANG ON CELLULAR FREE CALCIUM AND ENDOTHELIN IN OBSTRUCTIVE JAUNDICE AND PROTECTIVE MECHANISM
     肝复康对阻塞性黄疸肝细胞游离钙和内皮素的影响及其肝保护作用机制
短句来源
  “肝细胞游离钙”译为未确定词的双语例句
     [WT5”HZ]Methods [WT5”BZ]The effect of Tet on cytoplasmic free calcium concentration ([Ca 2+ ]i) was studied with Fura 2/AM in isolated rats' hepatocytes.
     方法  (1)Fura- 2 AM检测Tet对离体肝细胞游离钙离子浓度 ([Ca2 + ]i)的影响。
短句来源
     Effect of Platelet - Derived Growth Factor on Intracellular Free Ca~(2+) Concentration in Hepatocytes
     血小板衍生生长因子对肝细胞游离钙浓度影响
短句来源
     Plasma ALT , TBA and liver MDA and the intracellular free calcium([Ca~(2+)]i) concentrations increased markedly after hepatic ischemia-reperfusionand reached maximal at 6h , but the amount of bile juice markedly decreased and rapidly droupped to the lowest at 2h.
     并分别检测血清ALT含量、血清TBA含量及肝细胞Na~+-K~+ATP酶活性、MDA含量及肝细胞游离钙离子浓度。
短句来源
  相似匹配句对
     Effects of Glucocorticoids Hormone on Intracellular Free Calcium in Liver Cells
     糖皮质激素对肝细胞游离的作用
短句来源
     Effect of Platelet - Derived Growth Factor on Intracellular Free Ca~(2+) Concentration in Hepatocytes
     血小板衍生生长因子对肝细胞游离浓度影响
短句来源
     Liver Cell Adenoma
     肝细胞腺瘤
短句来源
     Effects of phenylephedrine on free calcium distribution in hepatocytes
     去氧肾上腺素对肝细胞游离分布的影响
短句来源
     Characteristics of free calcium distribution and Ca~(2+) oscillations in the subregeon of hepatocytes.
     肝细胞游离分布及振荡的亚细胞特征
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  cellular free calcium
Bile acids increase cellular free calcium in cultured kidney cells (LLC-PK1)
      
It is determined that bile acids alter cellular free calcium (Cai) levels in LLC-PK1 cells.
      
In our study, exposure to 150 M H2O2 induces a rapid 4to 5-fold elevation of the cellular free calcium levels within 30 min.
      
Regions present in both 2B and 2C are necessary to augment cellular free calcium levels.
      
This may lead to higher cellular free calcium levels and the activation of a variety of possible target cells.
      
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Objective [WT5”BZ]To investigate the protective effect and mechanism of tetrandrine (Tet) on ischemia reperfusion injury of the livers in rats. [WT5”HZ]Methods [WT5”BZ]The effect of Tet on cytoplasmic free calcium concentration ([Ca 2+ ]i) was studied with Fura 2/AM in isolated rats' hepatocytes. And Tet (8 mg/kg) was infused via vein before ischemia and 10 min before reperfusion, respectively. The serum alanine aminotransferase (ALT) and lactate dehydrogenase (LDH), and the liver tissue ATP, endurance...

Objective [WT5”BZ]To investigate the protective effect and mechanism of tetrandrine (Tet) on ischemia reperfusion injury of the livers in rats. [WT5”HZ]Methods [WT5”BZ]The effect of Tet on cytoplasmic free calcium concentration ([Ca 2+ ]i) was studied with Fura 2/AM in isolated rats' hepatocytes. And Tet (8 mg/kg) was infused via vein before ischemia and 10 min before reperfusion, respectively. The serum alanine aminotransferase (ALT) and lactate dehydrogenase (LDH), and the liver tissue ATP, endurance capacity (EC), endothelin (ET) and [Ca 2+ ]i were measured before and at the end of ischemia, and at 10 min and 50 min after reperfusion. [WT5”HZ] Results [WT5”BZ] The increase of [Ca 2+ ]i induced by ATP was significantly inhibited by Tet in a concentration dependent manner ( P <0.01). After reperfusion, the levels of ALT, LDH, ET, and [Ca 2+ ]i were significantly higher in the control group than those of the Tet group ( P <0.05), whereas, the levels of ATP and EC and the 5 day survival rate in the Tet group were significantly higher than those of the control group ( P < 0.01 ). Compared with the control group, nearly normal architecture was observed and ultrastructural damage was slight in the Tet group. [WT5”HZ] Conclusions [WT5”BZ] Tet can protect rats' livers against ischemia reperfusion injury, and the protective mechanism might be that it can selectively block the receptor operated Ca 2+ channel to decrease the Ca 2+ over loading.

目的 观察粉防己碱 (Tet)对大鼠肝再灌注损伤的防护作用及其机制。 方法  (1)Fura- 2 AM检测Tet对离体肝细胞游离钙离子浓度 ([Ca2 + ]i)的影响。 (2 )制作大鼠缺血再灌注损伤模型。将实验大鼠随机分为对照组 (Ctrl,鼠数 =35 )、粉防己碱 (Tet)组 (鼠数 =35 )和假手术组(Sham ,鼠数 =5 )。Tet组大鼠按 8mg kgTet于缺血前、再灌注前静脉注射 ,动态观察血清谷丙转氨酶 (ALT)、乳酸脱氢酶 (LDH)、肝组织三磷酸腺苷 (ATP)及能荷 (EC)、血浆内皮素 (ET)、肝细胞[Ca2 + ]i和肝组织学变化 ,并计算生存率。 结果 Tet能抑制ATP诱导细胞 [Ca2 + i]的增加 ,呈剂量依赖性 (P <0 .0 1)。再灌注后Tet组与Ctrl组相比 ,ALT、LDH、ET降低 (P <0 .0 5 ) ,ATP、EC增高(P <0 .0 1) ;再灌注末 [Ca2 + ]iTet组低于Ctrl组 (P <0 .0 1) ,Tet组肝组织破坏轻于Ctrl组 ,生存率高于Ctrl组 (P <0 .0 1)。 结论 Tet对大鼠...

目的 观察粉防己碱 (Tet)对大鼠肝再灌注损伤的防护作用及其机制。 方法  (1)Fura- 2 AM检测Tet对离体肝细胞游离钙离子浓度 ([Ca2 + ]i)的影响。 (2 )制作大鼠缺血再灌注损伤模型。将实验大鼠随机分为对照组 (Ctrl,鼠数 =35 )、粉防己碱 (Tet)组 (鼠数 =35 )和假手术组(Sham ,鼠数 =5 )。Tet组大鼠按 8mg kgTet于缺血前、再灌注前静脉注射 ,动态观察血清谷丙转氨酶 (ALT)、乳酸脱氢酶 (LDH)、肝组织三磷酸腺苷 (ATP)及能荷 (EC)、血浆内皮素 (ET)、肝细胞[Ca2 + ]i和肝组织学变化 ,并计算生存率。 结果 Tet能抑制ATP诱导细胞 [Ca2 + i]的增加 ,呈剂量依赖性 (P <0 .0 1)。再灌注后Tet组与Ctrl组相比 ,ALT、LDH、ET降低 (P <0 .0 5 ) ,ATP、EC增高(P <0 .0 1) ;再灌注末 [Ca2 + ]iTet组低于Ctrl组 (P <0 .0 1) ,Tet组肝组织破坏轻于Ctrl组 ,生存率高于Ctrl组 (P <0 .0 1)。 结论 Tet对大鼠肝缺血和再灌注损伤有明显的防护作用 ,其机制可能为选择性阻断肝细胞膜上受体操纵性钙通道 ,抑制细胞内Ca2 + 超载。

Objective To investigatetheeffectsof induciblenitricoxide(NO)andexogenousNO on theintracellularhome-ostasisof thehepatocytes.Methods EndogenousNOwasinducedby combinedactionof lipopolysaccharide(LPS)andcy-tokinesin culturedrathepatocytes,andexogenousNO was suppliedby sodiumnitroprusside(SNP)to stimulatethehepato-cytes.Thechangesin intracellularmalondialdehyde(MDA),reducedglutathione(GSH)andfreecalcium([Ca 2+ ] i )wereob-served.Results A substantialincreaseby7.97timesinintracellularMDAlevelanda decreaseby57.9%inGSHoccurredin...

Objective To investigatetheeffectsof induciblenitricoxide(NO)andexogenousNO on theintracellularhome-ostasisof thehepatocytes.Methods EndogenousNOwasinducedby combinedactionof lipopolysaccharide(LPS)andcy-tokinesin culturedrathepatocytes,andexogenousNO was suppliedby sodiumnitroprusside(SNP)to stimulatethehepato-cytes.Thechangesin intracellularmalondialdehyde(MDA),reducedglutathione(GSH)andfreecalcium([Ca 2+ ] i )wereob-served.Results A substantialincreaseby7.97timesinintracellularMDAlevelanda decreaseby57.9%inGSHoccurredin thehepatocytesafterthecellshadbeenincubatedwithLPSandcytokinesfor24h,whichwerereversedby43.5%and98.4%respectivelyby treatmentwithN G -monomethyl-L-arginine(NMMA),a competitivenitricoxidesynthase(NOS)inhibitor.Ver-apamilsignificantly reducedbothendogenousNO productionandoxidativestress,whiletheeffectof A23187was notcon-spicuous.IncubationwithchlorpromazineandVitamineE(VitE),however,didnotresultindecreasedreleaseof NO by LPS-andcytokines-inducedhepatocytes.AfterSNPexposureof thehepatocytes,theoxidativestatuswas reversiblyenhancedin a time-dependentmanner.Shortexposureto SNPledto a concentration-dependentinhibitionof therapidandtransientincrease infreecalciuminducedby K + depolarizationandhepatopoietin-coupledcalciummobilization.Con clusions InducibleNOmay initiateandplaya keyrolein thelatterstagesof metabolicandfunctionalstressresponsesof hepatocytesagainstendotoxin andcytokines,whenthereductionoccursin thecapacityof NO to independentlymediatelipidperoxidationandcounteract oxidation.Theinhibitoryeffectof NO on[Ca 2+ ] i mobilizationmaybe an importantautoregulatorymechanismby meansof negativefeedbackon proteinkinaseC-associatedNOSinduction.

目的研究肝细胞诱导性一氧化氮(NO)及外源性NO对肝细胞内环境稳定的影响。方法用内毒素及细胞因子诱导培养大鼠肝细胞内源性NO及应用外源NO供体硝普钠(SNP)与原代肝细胞作用,观察肝细胞丙二醛(MDA)、还原型谷胱苷肽(GSH)及细胞内游离钙的变化规律。结果内毒素+细胞因子作用肝细胞24h后,肝细胞MDA增高7.97倍及GSH降低57.9%,一氧化氮合酶(NOS)竞争性抑制剂NG-甲基-L-精氨酸使肝细胞MDA及GSH分别逆转43.5%和98.4%。异搏定显著抑制内源性NO合成及相关氧应激,A23187的作用不显著,而氯丙嗪和α-生育酚并不导致内毒素+细胞因子诱导肝细胞释放的NO下降。SNP作用肝细胞表现为可逆性增强氧化态,但外源NO显著抑制K+去极化及肝细胞生长素诱导动员的肝细胞游离钙瞬增。结论在内毒素及细胞因子导致肝细胞代谢和功能应激反应中,诱导NO、独立介导脂质过氧化和抗氧化能力下降,可能具有起始关键作用;NO抑制肝细胞内游离钙动员,可能通过负反馈调节与蛋白激酶C相关的NOS诱导而作为一种重要的肝细胞内伺服调控机制。

 
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