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作 者:陈姝 [1] 陆惠民 [1] 高琪 [2] 张山鹰 唐学恒 [1] 孙臻安 [1]
机构地区:[1]苏州大学医学院寄生虫学教研室,江苏苏州,215007 [2]江苏省寄生虫病防治研究所 [3]福建省寄生虫病防治研究所
出 处:《中国寄生虫病防治杂志》2004年第3期151-154,共4页Chinese Journal of Parasitic Disease Control
基 金:江苏省自然科学基金资助项目 (No .BK971 57)
摘 要:目的 探讨NO在IL 12诱导抗伯氏疟原虫 (P .b)感染免疫效应中的作用。 方法 每只BALB/c小鼠接种 5× 10 5个感染P .b的RBC ,分组后分别给予 5mg/dNO合成酶选择性抑制aminoguanidine、0 .0 3 μg/dIL 12和aminoguani dine联合IL 12处理。观察各组小鼠原虫血症变化及生存时间。感染第 5d收集小鼠血清进行NO水平测定。 结果 aminoguanidine联合IL 12处理组小鼠的原虫血症水平与单独IL 12组差异不明显 ,却使小鼠生存率显著降低 ;IL 12联合aminoguanidine处理组较单独aminoguanidine及感染对照组原虫血症达峰值的时间显著推迟 ,小鼠存活时间明显延长。IL 12处理小鼠血清NO水平显著上升 ;给予aminoguanidine后的小鼠血清NO含量较低 ,与感染对照组水平接近。 结论 aminoguanidine能有效的抑制IL 12诱导的NO的产生 ,显著降低IL 12处理小鼠生存率 ,但对原虫血症水平无明显影响。因此 ,IL 12抗P .b感染的免疫保护作用部分依赖NO介导 ,且NO的作用可能并非是NO对疟原虫的直接杀伤。Objective To explore the role of NO in IL-12-induced resistance to Plasmodium berghei infection. Methods BALB/c mice were infected with 5×10 5 parasitized RBC each mouse and divided into four groups. Four groups of mice were treated with 0.03 μg/d of IL-12,5 mg/d of aminoguanidine,IL-12 plus aminoguanidine and PBS respectively. The course of parasitemia was determined on the days indicated and survival time was calculated until death for each group of mice. Mice sera were collected on day 5 post-infection and levels of NO in sera were detected. Results There were no significant differences in the levels of parasitemia between mice of IL-12 group and those of IL-12 plus aminoguanidine group,but significant decreases in survival rate were observed among mice of IL-12 plus aminoguanidine group compared with those of IL-12 group. However,the mice of IL-12 plus aminoguanidine group significantly delayed the peak of parasitemia and prolonged survival time in comparison with aminoguanidine and control groups. In addition,treatment of IL-12 alone resulted in profound increase in the serum level of NO,but when combination of IL-12 with aminoguanidine,led to marked decrease in the level of NO,which comparable with control. Conclusion The results demonstrated that aminoguanidine could abrogate IL-12-induced NO production and significantly decreased the survival rate of infected mice,but has no effect on parasitemia. Therefore,these results also provide strong evidence that IL-12-induced resistance against P. berghei occurs in part by a NO-dependent mechanism. However,the effect of NO may be other than antiparasite.
关 键 词:白细胞介素12 疟原虫 伯氏 NO合成酶选择性抑制剂 一氧化氮
分 类 号:R382.31[医药卫生—医学寄生虫学]
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