Guidot D M, Linas S L, Repine M J, Shanley P F, Fisher H S, Repine J E
Webb-Waring Institute for Biomedical Research, Department of Medicine, Denver General Hospital, University of Colorado Health Sciences Center.
Inflammation. 1994 Oct;18(5):537-45. doi: 10.1007/BF01560700.
Hearts from rats treated with interleukin-1 (IL-1) intraperitoneally developed a rapid (6 h after IL-1), transient increase in neutrophils, tissue hydrogen peroxide (H2O2), and oxidized glutathione (GSSG) levels, and a subsequent (36 h after IL-1) increase in myocardial glucose-6-phosphate dehydrogenase (G6PD) activity and tolerance to ischemia-reperfusion. In the present investigation, we found that rats treated similarly with IL-1 had increased numbers of neutrophils in their kidneys, which were comparable to myocardial neutrophil increases, but did not develop increased renal tissue H2O2 or GSSG levels acutely (6 h after IL-1) or increased G6PD activity or resistance to ischemia-reperfusion injury later (36 h after IL-1). Our findings indicate that IL-1 treatment increased neutrophil accumulation in rat kidneys but did not increase oxidative stress, antioxidant enzyme activity, or resistance to ischemia-reperfusion injury. We conclude that organ-to-organ differences exist with respect to IL-1-induced tolerance.
经腹腔注射白细胞介素-1（IL-1）处理的大鼠心脏，在注射后6小时出现中性粒细胞、组织过氧化氢（H2O2）和氧化型谷胱甘肽（GSSG）水平迅速短暂升高，随后（注射后36小时）心肌葡萄糖-6-磷酸脱氢酶（G6PD）活性增加，对缺血再灌注的耐受性增强。在本研究中，我们发现，经同样处理的IL-1大鼠肾脏中的中性粒细胞数量增加，与心肌中性粒细胞增加情况相当，但在急性阶段（注射后6小时）肾脏组织H2O2或GSSG水平未升高，后期（注射后36小时）G6PD活性或对缺血再灌注损伤的抵抗力也未增加。我们的研究结果表明，IL-1处理可增加大鼠肾脏中的中性粒细胞积聚，但不会增加氧化应激、抗氧化酶活性或对缺血再灌注损伤的抵抗力。我们得出结论，在IL-1诱导的耐受性方面存在器官间差异。
