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肝细胞缺氧
相关语句
  hepatocyte hypoxic
     Effect of protein kinase C during hepatocyte hypoxic precondition
     蛋白激酶C在肝细胞缺氧预处理中的作用
短句来源
     Induction of HSP70 during hepatocyte hypoxic preconditioning
     肝细胞缺氧预处理细胞保护作用中热休克蛋白70表达的调控机制
短句来源
  “肝细胞缺氧”译为未确定词的双语例句
     Influence of Se on Oxygen-deficiency Damage of Human Liver Cells
     硒对人肝细胞缺氧-复氧损伤的影响
短句来源
     Anti-apoptotic effect of hypoxia pretreatment on liver cell line L02 of hypoxia/reoxygenation injury
     缺氧预处理对L02肝细胞缺氧复氧损伤的抗凋亡保护作用
短句来源
     Objective To investigate the relationship between the expression of HSP70 and hypoxic preconditioning (HP) and the modulatory mechanism.
     目的 研究热休克蛋白 70 (HSP70 )表达与肝细胞缺氧预处理的关系及其调控机制。
短句来源
     Objective To investigate the impact of lidocaine preconditioning on the expression of Bcl-2,Caspase-3 in liver cell and apoptosis during hypoxia-reoxygenation injury.
     目的探讨利多卡因预处理对肝细胞缺氧/复氧后Bcl-2、Caspase-3蛋白表达及细胞凋亡的影响。
短句来源
     Methods Through a normal liver cell IP model,PKC inhibitor,activator and MEK inhibitor were utilized to analyze the phosphorylation of PKC and P44/42 MAPKs. The cellular ultrastructure,HSP expression and viability were also observed.
     方法:建立体外肝细胞缺氧预处理模型,应用PKC抑制剂、激动剂和丝分裂原激活的蛋白激酶激酶(mitogen-activated protein inase klnase,MEK)抑制剂,通过检测PKC和P44/42 MAPKS磷酸化水平,HSP70的表达量,细胞活力,以及电镜下观察细胞形态结构的损伤较轻。
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  相似匹配句对
     The Effects of Hypoxia on Polarity of Hepatocytes Cultured in Vitro
     缺氧对培养肝细胞极性的影响
短句来源
     Hypoxia was attenuated after transformation from cirrhosis to HCC.
     肝细胞癌变后缺氧程度减轻。
短句来源
     Liver Cell Adenoma
     肝细胞腺瘤
短句来源
     2) hypoxia (H);
     (2)缺氧组;
短句来源
     Cold and Hypoxia
     低温与缺氧
短句来源
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Objective To study the protective effect of fructose with regard to hypoxia induced hepatocytes injury during the long microencapsulation periods. Methods Eighteen SD rats were divided into three groups, 6 rats each. In group A, fructose was added into the perfusion solutions (20?mmol/L). There was no fructose in group B and C. After isolation and microencapsulation, the viability was tested. In vitro culture, fructose (10?mmol/L) was added in culture medium in group C, but not in groups A and B. LDH leakage...

Objective To study the protective effect of fructose with regard to hypoxia induced hepatocytes injury during the long microencapsulation periods. Methods Eighteen SD rats were divided into three groups, 6 rats each. In group A, fructose was added into the perfusion solutions (20?mmol/L). There was no fructose in group B and C. After isolation and microencapsulation, the viability was tested. In vitro culture, fructose (10?mmol/L) was added in culture medium in group C, but not in groups A and B. LDH leakage and TP of culture were examined.Results The survival of hepatocytes in group A was obviously higher than in groups B and C ( P < 0.01 ). The LDH leakage in group A was significantly lower than in groups B and C ( P < 0.01 ).Conclusion Fructose could protect hepatocytes against hypoxia induced cell damage during microencapsulation, but cells should be pre treated with fructose before hypoxia.

目的 为了减少肝细胞在微囊化过程中的缺氧损伤, 研究在缺氧状态下果糖对肝细胞的保护作用。方法 将SD大鼠分为三组:A 组, 细胞分离的灌流液和消化液中均加果糖20 m mol/L,B、C两组不加果糖; 细胞分离及微囊化后, 检测细胞的活率; 微囊化肝细胞行体外培养,C组培养液中加果糖10 m mol/L,A、B两组不加。测定三组肝细胞的乳酸脱氢酶(LDH) 漏出率( % ) 及培养上清液中的总蛋白质。结果 A组的细胞活率显著高于B、C 两组( P< 0 .01) , 而A 组的LDH 漏出率显著低于B、C组( P< 0 .01) ,A 组蛋白质合成功能的恢复显著优于B、C 组( P< 0 .01) 。结论 果糖在缺氧状态下能有效延缓肝细胞的缺氧损伤, 但应在缺氧状态发生之前给予才能发挥作用。

The model of oxygen_deficiency and oxygen_restoration damage of liver cells was established.The influence of Se on oxygen-deficiency damage of liver cells was studied.The results showed that Se had protective effects on human liver cells.

建立人肝细胞缺氧-复氧损伤模型,观察了微量元素硒的保护作用。结果表明,模型组肝细胞内、外丙二醛水平均显著增高,丙氨酸转氨酶外释增多,白蛋白合成减少,与正常对照组比较,差异有显著性意义(P<001)。1156×10-7mol/L硒预保护组上述损伤变化明显减轻(P<005)。揭示硒对缺氧-复氧所致人肝细胞脂质过氧化损伤具有保护作用。

Objective To observe the effects of hypoxia caused by trauma on glucose aerobic metabolism in cultured rat liver cells. Methods Cells were exposed to different concentrations of oxygen to simulate hypoxic state after trauma, and then the activities of enzymes related to glucose aerobic metabolism in hepatocytes were determined. Hepatocytes cultured under normal condition were used as normal control. Results Compared with those of the normal control group, the activities of PDH, KGDH, CCO were significantly...

Objective To observe the effects of hypoxia caused by trauma on glucose aerobic metabolism in cultured rat liver cells. Methods Cells were exposed to different concentrations of oxygen to simulate hypoxic state after trauma, and then the activities of enzymes related to glucose aerobic metabolism in hepatocytes were determined. Hepatocytes cultured under normal condition were used as normal control. Results Compared with those of the normal control group, the activities of PDH, KGDH, CCO were significantly lower under different hypoxic conditions, especially in 1% O 2 group. Conclusion Glucose aerobic metabolism and production of ATP are inhibited by hypoxia.

目的 观察缺氧对肝脏实质细胞糖有氧氧化的影响。方法 利用体外培养的肝细胞缺氧模型 ,模拟创伤后的缺血、缺氧状态 ,以正常培养的大鼠肝细胞为对照 ,采用生物化学的方法 ,分析不同氧浓度及缺氧时间下肝细胞有氧氧化关键酶活性的变化 ,并测定了细胞内ATP含量的变化。结果 与正常对照组相比 ,缺氧肝细胞内丙酮酸脱氢酶 (PDH)、α 酮戊二酸脱氢酶 (KGDH)、细胞色素C氧化酶 (CCO)活性在缺氧培养 1h即显著降低 ,并持续到 16h ;缺氧时肝细胞内ATP含量随时间延长而下降 ,4h达到最低。结论 缺氧后肝细胞有氧氧化及细胞内ATP的产生严重受抑

 
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