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作 者:王丽[1] 李惊子[1] 赵志辉[1] 李健[1] 王海燕[1] 陈德文[1] 陆道惠[1]
机构地区:[1]北京医科大学第一医院肾内科,北京医科大学肾脏病研究所,中国科学院化学研究所
出 处:《中国病理生理杂志》1996年第4期369-369,共1页Chinese Journal of Pathophysiology
基 金:国家自然科学基金
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.
分 类 号:R692.310.2[医药卫生—泌尿科学]
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