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cyclooxygenase-     
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  cyclooxygenase-
3D QSAR ANALYSIS OF SOME HETEROCYCLIC COMPOUNDS AS CYCLOOXYGENASE-2 INHIBITORS
      
These studies may be useful in designing molecules with better cyclooxygenase-2 inhibitory activity.
      
Evidence for an essential role of cyclooxygenase-2 as a mediator of the late phase of ischemic preconditioning in mice
      
Recent studies have demonstrated that cyclooxygenase-2 (COX-2) is an essential mediator of the cardioprotective effects of the late phase of ischemic preconditioning (PC) in rabbits.
      
Subsequently, this cascade of reactions modulates a plethora of cardioprotective proteins including heat shock proteins, KATP channels, nitric oxide synthase, cyclooxygenase-2, and antioxidants.
      
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Cyclooxygenase-2(COX- 2) is an inducible cyclooxygenase which may Play an important role in in-flammatory diseases.METHODS: To examine the involvement of COX-2 in the inflammatory renal diseases in vivo the expression of this was detected in kidneys of mice that receiving unilateral ureteral obstruction(UUO) at 4-hours, 24-hours, 72 - hours, 5-day, 7-dsys by RT - PCR methed. The morphological changes of the obstructed kidneys wereobserved at the same time point. RESULTS:The regults demonstrated...

Cyclooxygenase-2(COX- 2) is an inducible cyclooxygenase which may Play an important role in in-flammatory diseases.METHODS: To examine the involvement of COX-2 in the inflammatory renal diseases in vivo the expression of this was detected in kidneys of mice that receiving unilateral ureteral obstruction(UUO) at 4-hours, 24-hours, 72 - hours, 5-day, 7-dsys by RT - PCR methed. The morphological changes of the obstructed kidneys wereobserved at the same time point. RESULTS:The regults demonstrated that the expression of COX-2 mRNA were beginningto imcrease at 4-hours , were up to peak at 72 -hare after UUO operation. A few numbers of infiltrating inflammatory cellswere found at 24 - hours, a large humbers of infiltration inflammatory cells were found 72 -hours, and the peak of the num-bers of those cells was at 7-days after UUO operation. CONCLUSIO: COX-2 expression is upreghated in the obstract-ed kidneys of UUO mice.The overexpression of COX-2 may be an inducing or promoting factor in inflammatory cells infil-tration in the kidney of UUO mice.

目的:观察环氧化酶-2(COX-2)在单侧输尿管梗阻小鼠梗阻肾脏内的表达情况,探讨COX-2在炎性肾脏疾病中清理生理作用。方法:利用阿-PCR检测了COX-2在小鼠单侧输尿管梗阻后4h、24h、72h、sd和7d的表达变化并采用PAS染色观察上述各时间点的肾组织病理改变。结果:单侧输尿管梗阻术后4h肾皮质中的COX-2的表达开始增高,72h达到高峰。术后第一天肾间质中可见少量炎细胞浸润,第3d明显增多,第7d达到高峰。结论:本研究提示COX-2的过度表达很可能是单侧输尿管便用后肾内炎细胞浸润和积聚的起站或促进因素之一。

To investigate the effects of arachidonate cyclooxygenation and 5 lipoxygenation on golmerular expression of the gene for inducible nitric oxide synthesase(iNOS)in rats with accelerated nephrotoxic serum nephritis(NSN). METHODOLOGY The model of NSN was established in male SD rats with peritoneal injection of rabbit IgG and Freund complete adjuvant followed by intravenous injection of anti rabbit GBM antibody.Rats of NSN were grouped into:(1)NSN group(...

To investigate the effects of arachidonate cyclooxygenation and 5 lipoxygenation on golmerular expression of the gene for inducible nitric oxide synthesase(iNOS)in rats with accelerated nephrotoxic serum nephritis(NSN). METHODOLOGY The model of NSN was established in male SD rats with peritoneal injection of rabbit IgG and Freund complete adjuvant followed by intravenous injection of anti rabbit GBM antibody.Rats of NSN were grouped into:(1)NSN group( n =8);(2)NSN+INDO group ( n =8)in which NSN rats were pretreated with indomethacin (3mg/kg,a cyclooxygenase inhibitor)intravenously one hour before the injection of anti GBM antibody;and (3) NSN+MK( n =8)group in which the NSN rats were pretreated with MK 0951(a 5 lipoxygenase inhibitor)intravenously one hour before the injection of anti GBM antibody.Six rats administered with normal rabbit serum were set as the control.HPLC and radioimmunoassay were used in the determination of prostaglandin E2(PGE 2),leukotrience B4(LTB 4)and thronmboxane B2(TXB 2).Glomerular expression of iNOS was determined by RNAase protection assay. RESULTS Enhanced glomerular synthesis of PGE 2 and TXB 2,increased the urinary excretion of nitrite (NO 2),and up regulated glomerular expression of iNOS mRNA were found in NSN group as compared to the control.In NSN+INDO group in which cyclooxygenation was inhibited,glomerular synthesis of PGE 2 and TXB 2 was suppresseds glomerular expression of iNOS enhanced,glomerular synthesis of LTB 4 and urinary excretion of NO 2 increased.Pretreatment of nephritic rats with MK 0951,a 5 lipoxygenase inhibitor,reduced the enhanced glomerular synthesis of LTB 4,stimulated the iNOS induction and increased the urinary excretion of NO 2. CONCLUSION These results indicated that cyclooxygenation and 5 lipoxygenation inhibit the expression of iNOS in glomeruli of rats with NSN.

目的:研究花生四烯酸( AA) 环氧化酶产物及5脂氧化酶产物对大鼠加速性肾毒性血清性肾炎( NSN) 中肾小球诱生型一氧化氮合成酶(iNOS) 表达的影响。 方法:制备NSN 大鼠模型后,应用消炎痛抑制AA环氧化酶,应用MK0951 抑制AA 的5脂氧化酶,观察对肾小球iNOS 表达的影响。 结果:在NSN 大鼠,应用消炎痛抑制环氧化酶,可减少肾小球合成的前列腺素(PG) E2 及血栓素( TX) B2 ,使肾小球iNOS 表达增强,尿亚硝酸盐( NO-2 ) 排出增多;应用MK0951 抑制5脂氧化酶,可减少肾小球合成的白三烯(LT) B4 ,也使肾小球iNOS 表达增强,尿NO-2 增多。 结论:NSN 大鼠肾小球合成的环氧化酶及5脂氧化酶产物PGE2 、TX 及LT 有抑制肾小球iNOS 表达的作用。

OBJECTIVE To investigate the effect of nitric oxide(NO)on glomerular synthesis of eicosanoids in accelerated nephrotoxic serum nephritis(NSN)in rats. METHODOLOGY Glomerular synthesis of prostaglandin(PG)E2,6 keto PGF12,thromboxane(TX)B2,leukotries(LT)B4,LTC4,5 hydroxyeicosatetraenoic acid(5 HETE),12 HETE,15 HETE were determined with high pressure liquid chromatography and radioimmunoassay.Rats of NSN were treated with L NIL,an inhibitor of inducible nitric oxide...

OBJECTIVE To investigate the effect of nitric oxide(NO)on glomerular synthesis of eicosanoids in accelerated nephrotoxic serum nephritis(NSN)in rats. METHODOLOGY Glomerular synthesis of prostaglandin(PG)E2,6 keto PGF12,thromboxane(TX)B2,leukotries(LT)B4,LTC4,5 hydroxyeicosatetraenoic acid(5 HETE),12 HETE,15 HETE were determined with high pressure liquid chromatography and radioimmunoassay.Rats of NSN were treated with L NIL,an inhibitor of inducible nitric oxide synthase(iNOS). RESULTS Glomerular synthesis of PGE2,6 keto PGF12,TXB2,LTB4,5 HETE and 15 HETE1 were enhanced in rats of NSN except LTC4.The enhanced glomerular synthesis of the eicosanoids were inhibited by the treatment with L NIL. CONCLUSION iNOS derived NO stimulates glomerular activity of cyclooxygenase,5 and 15 lipoxygenases,promotes the syntheses of PEG2,PGI2,LTB4,5 HETE and 15 HETE that might be involved in the pathogenesis of NSN.

目的:探讨一氧化氮(NO)在实验性肾小球肾炎中对肾小球花生四烯酸(AA)产物合成的调节作用。方法:制备大鼠加速性肾毒性肾炎(NSN)模型,应用高效液相层析及放免法测定肾小球合成的前列腺素(PG)E2、6酮PGF1α、血栓素(TX)B2、白三烯(LT)B4、LTC4、5羟二十碳四烯酸(5HETE)、12HETE、15HETE。对NSN大鼠应用诱生型NO合成酶(iNOS)抑制剂LNIL处理。结果:在NSN大鼠,肾小球合成的上述AA产物中除LTC4外均升高,应用LNIL可抑制其中PGE2、6酮PGF1α、LTB4、5HETE、15HETE的升高。结论:iNOS衍生的NO激活肾小球的环氧化酶、5脂氧化酶及15脂氧化酶,促进部分AA产物合成,从而参与肾小球肾炎的发病,证实NO为肾小球AA产物合成的调节因子。

 
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