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鼠脑型疟疾的发展并不需要一氧化氮的产生。

The development of murine cerebral malaria does not require nitric oxide production.

作者信息

Favre N, Ryffel B, Rudin W

机构信息

Department of Medical Parasitology, Swiss Tropical Institute, Basel, Switzerland.

出版信息

Parasitology. 1999 Feb;118 ( Pt 2):135-8. doi: 10.1017/s0031182098003606.

Abstract

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 by 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.

摘要

一氧化氮(NO)的产生被认为是脑型疟疾发展所必需的。然而,这种分子对于这种病理表现的重要性存在争议。为了评估鼠脑型疟疾是否依赖于NO,我们研究了可诱导型一氧化氮合酶(iNOS)缺陷小鼠中血期伯氏疟原虫ANKA(PbA)感染的进程。寄生虫血症、血液学改变、脑型疟疾的存活和发展不受iNOS缺乏的影响。为了排除其他一氧化氮合酶产生的NO的作用,对照组包括口服氨基胍(AG,一种一氧化氮合酶抑制剂)来抑制NO。与iNOS缺陷小鼠一样,AG治疗后在寄生虫血症进程、存活和血液学值方面未观察到差异。我们的结果表明,NO的产生不是鼠脑型疟疾发展的关键因素。

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