摘要
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。
h after the injection of nephroto xic serum to the accelerated nephrotoxicserum nephritic rat model,the free hydroxyl radical and IL-1 activity produeed byglomerular macrophages(GMφ),own peritoneal Mφ(PMφ),and normal peritoneal Mφ(N-PMφ)were detected by electron spin resonance(ESR)and thymocyte proliferation. Theeffect of IL-1 on production of free hydroxyl radical by rat GMφ and PMφand N-PMφwas also observed.The resuIts showed that IL-1 activity and hydroxyl radical insupernatants of GMφ of the experimental group was significantly higher than that of ownPMφ and N-PMφ,Free hydroxyl radical production in GMφ stimulated by rIL-1 was in-creased more than that of PMφ and N-PMφ significantly.These results suggested that theoveractivity of infiltrated Mφ in inflammatory glomeruli produeed large quantity of IL-1,furthermore IL-1 stimulated GMφ to produce more reactive oxygen,This vicious circle inlocal glomeruli may play an important role in the pathogenesis of renal injury inaccelerated nephrotoxic nephritis.
出处
《中国病理生理杂志》
CSCD
北大核心
1996年第4期369-369,共1页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
