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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 regulatory effect of nitric oxide (NO) on the synthesis of arachidonic acid (AA) in glomerulonephritis in experimental glomerulonephritis. Methods: The rat model of accelerated nephrotoxic nephritis (NSN) was prepared. The contents of prostaglandin (PG) E2, 6ketonePGF1α, TXB2, Leukotriene (LT) B4, LTC4, 5-hydroxyeicosatetraenoic acid (5-HETE), 12-HETE, 15-HETE. NSN rats with inducible NO synthase (iNOS) inhibitor L NIL treatment. RESULTS: In NSN rats, the above AA products of glomerulus were all elevated except LTC4, L-NIL could inhibit the increase of PGE2, 6-PGF1α, LTB4,5-HETE and 15-HETE . CONCLUSIONS: iNOS-derived NO activates glomerular cyclooxygenase, 5-lipoxygenase and 15-lipoxygenase to promote the synthesis of some AA products and thus participate in the pathogenesis of glomerulonephritis, confirming that NO is glomerular AA Modulation of product synthesis.