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hepatic membrane
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  肝膜
     THE EFFECT OF ESTROGEN ON SERUM LIPOPROTEINS AND HEPATIC MEMBRANE LDL RECEPTOR IN RATS
     雌激素对大鼠血清脂蛋白和肝膜LDL受体的影响
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  肝细胞膜
     Relationship between hepatic membrane protein MRP3 and nuclear receptor RXRα
     阻塞性胆汁淤积大鼠肝细胞膜蛋白MRP3与核受体RXRα蛋白表达关系的研究
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     The equilibrium constant of association(Ka) was (3 49±0 24)×10 10 (mol/L) -1 , and the binding capacity(Bmax) was 146 8±10 6 fmol/mg protein. The results suggested that the specific binding of brGH to black seabream hepatic membrane had properties which are in agreement with the characteristics of hormone receptors. Therefore, a sensitive GH radioreceptor assay(RRA) was developed.
     Scachard作图分析表明黑鲷肝细胞膜蛋白存在brGH单一的高亲和结合位点 ,Ka为 (3 49± 0 2 4)× 10 10 (mol/L) -1,Bmax为 146 8± 10 6fmol/mgprotein。
短句来源
     Conclusion The up-regulation of hepatic membrane protein MRP3 may be associated with down-regulation of nuclear receptor RXRα.
     结论肝细胞膜蛋白MRP3表达的上调可能与核受体RXRα表达抑制有关。
短句来源
     Only about 40% of the bound 125 I brGH could dissociate from its binding sites even after 24 hour of incubation, suggesting that the binding of brGH to black seabream hepatic membrane was only partly reversible.
     (2 )可饱和性 12 5I brGH与黑鲷肝细胞膜蛋白的特异性结合随着膜蛋白浓度或12 5I brGH加入量的上升而呈逐渐上升并达到饱和状态的趋势 ;
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     Objectiv To observe the effects of some traditional Chinese medical herbs such as Coptidis Rhizoma, Hirudo seu Whitmania, Raphani Semen on the receptor of hepatic membrane from the model of hypertensive insulin resistance rats.
     目的观察中药黄连、水蛭、莱菔子对高血压胰岛素抵抗模型大鼠肝细胞膜胰岛素受体的影响。
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  “hepatic membrane”译为未确定词的双语例句
     reduce the content of Chol, SM and elevate PC, PE of hepatic membrane;
     降低肝Cho1、SM含量,提高PC、PE含量;
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     Results:Compared with normal control group,model control group appeared to be significantly enlarged in MDA and membrane fluorescence polarization degree,and it was correlate with the normal control group(r=0 9651,r=0 9746),which showed hepatic membrane fluidity was reduced by lipid peroxidation;
     结果 :模型对照组MDA、膜荧光偏振度较正常组明显增大 ,且二者呈正相关 (r=0 96 5 1、r =0 974 6 ) ,表示肝脏因脂质过氧化引起膜流动性降低 ;
短句来源
     Objective To investigate the relationship between the hepatic membrane protein MRP3(multidrug resistance-associated protein 3,MRP3) expression and the nuclear hormone receptor RXRα(retinoid-X receptor alpha,RXRα)expression in both cultured hepatoma cell HepG2 and bile duct ligated(BDL) rat liver.
     目的通过体外细胞培养和建立大鼠胆管结扎(b ile duct ligation,BDL)所致阻塞性胆汁淤积动物模型,在蛋白水平观察多耐药相关蛋白MRP3(mu ltidrug resistance-assoc iated prote in 3,MRP3)和核受体RXRα(retinoid-X receptor al-pha,RXRα)表达的关系。
短句来源
     According to the results mentioned above, we proposed that HSS should havean antioxidative effect on the hepatic membrane lipid peroxidation which wasincreased by free radicals produced by CCl_4. In addition, HSS might increaseantioxidative ability of hepatocyte and stimulate the proliferation of hepatocy-tes.
     这些结果提示,HSS具有抗氧化作用,能抗CCl_4所产生的自由基对膜脂质的过氧化。 此外还加强肝细胞本身抗氧化能力和促进受损肝脏再生。
短句来源
     The radioreceptor binding assay showed that haw and flavonoids could increase hepatic LDLR density,but could not change the affinity of LDL to hepatic membrane LDLR.
     放射性配体结合力试验表明 ,山楂及山楂黄酮显著增加了大鼠肝脏 LDLR数目 ,而对亲和力影响不明显。
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  hepatic membrane
Hepatic Membrane Transport of Organic Cations Using Isolated Rat Hepatocyte Membrane Vesicles: Structure-Transport Relationships
      
Analysis of hepatic membrane cholesterol shows that ethanol induced a slight increase in microsomes exclusively due to free cholesterol while mitochondria was not affected.
      
Influence of circulating GH levels on GH-binding capacity measurements in the hepatic membrane of rainbow trout (Oncorhynchus my
      
TNF-a, IL-6, and hepatic membrane potentials (Em) were obtained.
      
TNF-a, IL-6, and hepatic membrane potentials (Em) were obtained.
      
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In our previous werk we have demonstrated a protective effect of hepaticstimulator substance (HSS) on experimental hepatic injury in mice. The un-derlying mechanism of this effect was further investigated with the following re-sults: (1) HSS could significantly increase the CCl_4-induced decrease of mem-brane fluidity of hepatic plasmalemma, mitochondria and microsomes to thecontrol level. (2) HSS could decrease the liver melondialdehyde contents ofCCl_4-intoxicated mice. (3) HSS could restore the liver glutathione...

In our previous werk we have demonstrated a protective effect of hepaticstimulator substance (HSS) on experimental hepatic injury in mice. The un-derlying mechanism of this effect was further investigated with the following re-sults: (1) HSS could significantly increase the CCl_4-induced decrease of mem-brane fluidity of hepatic plasmalemma, mitochondria and microsomes to thecontrol level. (2) HSS could decrease the liver melondialdehyde contents ofCCl_4-intoxicated mice. (3) HSS could restore the liver glutathione contentslowered by CCl_4-intoxication. (4) HSS stimulated regeneration of liver, enhan-ced DNA synthesis of hepatocytes and increased ~3H-TdR incorporation into DNA.According to the results mentioned above, we proposed that HSS should havean antioxidative effect on the hepatic membrane lipid peroxidation which wasincreased by free radicals produced by CCl_4. In addition, HSS might increaseantioxidative ability of hepatocyte and stimulate the proliferation of hepatocy-tes. These protective mechanisms might act in a concordant manner.

我们前文证明肝再生刺激因子(HSS)对小鼠实验性肝损伤有保护作用。本文进一步探讨其机制并获得如下结果:(1)HSS显著提高由CCl_4所降低肝细胞膜、线粒体膜和微粒体膜的流动性,使其上升到对照水平。(2)HSS使CCl_4所致的肝组织丙二醛升高幅度降低。(3)HSS使CCl_4所致的肝组织谷胱甘肽降低的含量回升。(4)HSS能刺激受CCl_4损伤的肝再生,促进肝细胞合成DNA和~3H-TdR掺入肝细胞DNA。这些结果提示,HSS具有抗氧化作用,能抗CCl_4所产生的自由基对膜脂质的过氧化。此外还加强肝细胞本身抗氧化能力和促进受损肝脏再生。这些保肝机制可能相互联系。

Rats treated with streptozocin (STZ 55 mg, iv, tail vein) induced diabetes then divided into 2 groups: diabetes (D), insulin-treated (T), other rats gaven vehicle as control (0). Two weeks later, plasma glucose, glomerular filtration rate (GFR) and plasma argirine vasopressin (AVP) were measured. 125I [d(CH2)5-Sarcosine7] AVP, a selective vasopressin V1 receptor antagonist was used as a redioligand in renal medulla and hepatic membrane binding stadies. GFR was increased in D and T groups (D = l6.98±2.56ml/min-1·kg-1,...

Rats treated with streptozocin (STZ 55 mg, iv, tail vein) induced diabetes then divided into 2 groups: diabetes (D), insulin-treated (T), other rats gaven vehicle as control (0). Two weeks later, plasma glucose, glomerular filtration rate (GFR) and plasma argirine vasopressin (AVP) were measured. 125I [d(CH2)5-Sarcosine7] AVP, a selective vasopressin V1 receptor antagonist was used as a redioligand in renal medulla and hepatic membrane binding stadies. GFR was increased in D and T groups (D = l6.98±2.56ml/min-1·kg-1, T= 15.49±0.99 ml/min-1·kg-1, C = 12.30±0.69ml/min-1·kg-1). AVP cor centration was elevated in D group (D = 8.22±0.85pg/ml, T = 7.01±0.42pg/ml, C = 6.55±0.82pg/ml). Binding studies showed that the kidney medullary membrane Bmax was unchanged in 8 groups but the Kd value was significantly higher in the D group than in the other groups(D = 0.89±0.06. T = 0.50±0.07, 0 = 0.50±0.08); hepatic membrane Bmax was increased in the T group (D = 85.20±16.5, T= 120±8.0, 0 = 98.0±13.0). We conclude that a lowered affinity of V1 receptors in diabetic rat is probably a factor causing increase in GFR. and a different mode of regulation of V1 receptors in the kidney and the liver was shown in this study.

本文利用链脲佐菌素诱导的实验性糖尿病大鼠,在糖尿病形成2周时分别测定血糖、肾小球滤过率(GFR)、血浆精氨酸血管加压素(AVP)、血钠及血浆渗透压,并用选择性AVP受体Ⅰ(V1)的放射配体~(125)I[d(CH_2)_5-Sarcosine~7]AVP对肾髓质膜和肝细胞膜V1受体进行结合分析。实验分三组:糖尿病组(D组)、胰岛素治疗组(T组)和对照组(C组)。结果表明,糖尿病形成2周时,各组血糖值为:D=37±7.5mmol/L;T=19±5.78mmol/L: C=7.63±0.59mmol/L。DT两组的GFR均增加,血浆AVP在D组明显高于对照组。膜受体结合试验显示:肾髓质膜V1受体最大结合容量(Bmax)在各组均无明显差异,解离常数(Kd值)D组大于T、C两组,肝细胞膜Bmax在T组增加,而Kd值在各组均未见改变。

The protective effect of coenzyme Q10 on liver damage in mice induced by the overdosage of Acetaminophen is reported. The results showed that CoQ10 decreased the activity of SALT, increased hepatic glycogen and ameliorated the pathological changes of hepatic damage due to overdosage of Acetaminophen in mice. It was also indicated that CoQ10could cause the increase of serum Acetaminophen concentration and glutathione content but did not change the content of hepatic microsome cytochrome P450. It could be concluded...

The protective effect of coenzyme Q10 on liver damage in mice induced by the overdosage of Acetaminophen is reported. The results showed that CoQ10 decreased the activity of SALT, increased hepatic glycogen and ameliorated the pathological changes of hepatic damage due to overdosage of Acetaminophen in mice. It was also indicated that CoQ10could cause the increase of serum Acetaminophen concentration and glutathione content but did not change the content of hepatic microsome cytochrome P450. It could be concluded that the mechanism of CoQ10 protective effect on hepatic damage induced by the overdosage of Acetaminophen might be regarded as the increase of stability of hepatic membrane and microsome membrane.

本文报道辅Q10(CoQ10)对超量AAP引起小鼠急性肝损伤的保护作用。结果表明,预先给小鼠皮下注射CoQ10,能对抗用量醋氨酚(AAP)所致的肝糖原含量下降和肝损伤引起的SALT活性升高及病理组织学变化;同时也发现CoQ10。能使血清AAP浓度和肝匀浆谷膦甘肽(GSH)含量高于对照组。这说明CoQ10对超量AAP所致的急性肝损伤确有保护作用。从后三项实验结果来看,CoQ10有间接稳定肝细胞膜的作用,使AAP毒性中间代谢产物生成减少。

 
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