The development of murine cerebral malaria does not require nitric oxide production
The development of murine cerebral malaria does not require nitric oxide production
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DOI：
10.1017/s0031182098003606
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发表时间：
1999-02-01
期刊：
影响因子：
2.4
通讯作者：
Rudin, W
中科院分区：
文献类型：
--
作者：
Favre, N;Ryffel, B;Rudin, W
一氧化氮（NO）的产生被认为是脑型疟疾发展所必需的。然而，这种分子对这种病理出现的重要性是有争议的。为了评估小鼠脑型疟疾是否依赖于NO，我们研究了诱导型一氧化氮合酶（iNOS）缺乏小鼠血期伯氏疟原虫ANKA （PbA）感染的过程。寄生虫病、血液学改变、脑疟疾的生存和发展不受iNOS缺乏的影响。为了排除其他NOS产生的NO的作用，对照包括通过口服氨基胍（AG）（一种NOS抑制剂）抑制NO。与inos缺陷小鼠一样，AG治疗后，寄生虫病病程、存活率和血液学指标均无差异。我们的研究结果表明NO的产生不是小鼠脑疟疾发展的关键因素。
Nitric oxide (NO) production has been suggested to be required for the development of cerebral malaria. However, the importance of this molecule for the appearance of this pathology is debated. To assess whether murine cerebral malaria is NO dependent, we investigated the course of blood-stage Plasmodium berghei ANKA (PbA) infections in inducible nitric oxide synthase (iNOS)-deficient mice. Parasitaemia, haematological alterations, survival and development of cerebral malaria were not affected by the: lack of iNOS. To exclude a role of NO produced by other NOS, controls included NO suppression bq oral administration of aminoguanidine (AG), a NOS inhibitor. As in iNOS-deficient mice, no difference in the parasitaemia course, survival and haematological values was observed after AG treatment. Our results indicate that NO production is not a crucial factor for the development of murine cerebral malaria.