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本文用大鼠加速肾毒血清肾炎模型，于注射肾毒血清后７２ｈ，用电子自旋共振（ＥＳＫ）和胸腺细胞增殖检测肾炎鼠的肾小球巨噬细胞（ＧＭφ），自身腹腔Ｍφ（ＰＭφ）及正常鼠腹腔Ｍφ（Ｎ－ＰＭφ）所产生羟自由基（ＯＨ）和ＩＬ－１活性。同时观察ＩＬ－１对ＧＭφ、ＰＭφ和Ｎ－ＰＭφ产生ＯＨ的影响。结果显示：肾炎鼠ＧＭφＩＬ－１活性和ｂＨ明显高于ＰＭφ和Ｎ－ＰＭφ；ＩＬ－１能刺激Ｍφ产生ＯＨ，且炎症ＧＭφ的ＯＨ明显高于ＰＭφ和Ｎ－ＰＭφ，揭示：肾小球中浸润的Ｍφ过度活化并产生大量ＩＬ－１及ＯＨ，ＩＬ－１又能进一步刺激Ｍφ产生更多的ＯＨ，这一肾小球内的局部恶性循环，在加速肾毒血清肾损伤的发病机制中可能起着重要作用。
Nephrotoxic serum nephritis model was accelerated in rats. At 72h after injection of nephrotoxic serum, glomerular macrophages (GMφ), peritoneal Mφ (PMφ) in nephritic rats were detected by electron spin resonance (ESK) and thymocyte proliferation. ) And normal mice (N-PMφ) produced by hydroxyl radical (OH) and IL-1 activity. Meanwhile, the effects of IL-1 on the OH production of GMφ, PMφ and N-PMφ were also observed. The results showed that the activity of GMφIL-1 and bH in nephritic rats were significantly higher than that in PMφ and N-PMφ; IL-1 could stimulate Mφ to produce OH, and the OH of inflammation GMφ was significantly higher than PMφ and N-PMφ, Mφ overactivation and produce a large number of IL-1 and OH, IL-1 can further stimulate Mφ to produce more OH, this local glomerular local vicious cycle in accelerating the pathogenesis of renal serum renal injury may Plays an important role.