摘要
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(5HETE)、12HETE、15HETE。对NSN大鼠应用诱生型NO合成酶(iNOS)抑制剂LNIL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LNIL可抑制其中PGE2、6酮PGF1α、LTB4、5HETE、15HETE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。
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.
出处
《肾脏病与透析肾移植杂志》
CAS
CSCD
1999年第2期116-118,共3页
Chinese Journal of Nephrology,Dialysis & Transplantation
基金
江苏省自然科学基金