Sanni L A
Division of Parasitology, National Institute for Medical Research, London, UK.
Redox Rep. 2001;6(3):137-42. doi: 10.1179/135100001101536238.
It has been suggested that sequestration of parasitized red blood cells might contribute to the pathogenesis of cerebral malaria (CM), by hypoxia causing either: (i) compensatory vasodilatation with a resultant increase in the brain volume; or (ii) enhancing cytokine-induced nitric oxide (NO) production via induction of inducible NO synthase (iNOS). Available evidence suggests that cerebral oedema is the initiating and probably the most important factor in the pathogenesis of murine CM. The relevance of this model in the study of the pathogenesis of CM has been questioned. However, a closer look at published reports on both human and murine CM, in this review, suggests that the pathogenesis of the murine model of CM might reflect more closely the CM seen in African children than that seen in Asian adults. It is also proposed that the role of iNOS induction during CM is protective: that the primary purpose of iNOS induction is to inhibit the side effects of brain indoleamine 2,3-dioxygenase (IDO) induction and quinolinic acid accumulation during hypoxia.
有人提出，被寄生的红细胞隔离可能通过以下缺氧情况导致脑型疟疾（CM）的发病机制：（i）代偿性血管扩张，导致脑容量增加；或（ii）通过诱导诱导型一氧化氮合酶（iNOS）增强细胞因子诱导的一氧化氮（NO）生成。现有证据表明，脑水肿是小鼠CM发病机制中的起始因素，可能也是最重要的因素。该模型在CM发病机制研究中的相关性受到了质疑。然而，在本综述中仔细研究关于人类和小鼠CM的已发表报告表明，CM小鼠模型的发病机制可能比亚洲成年人的CM更能紧密反映非洲儿童的CM。还提出CM期间iNOS诱导的作用是保护性的：iNOS诱导的主要目的是抑制缺氧期间脑吲哚胺2,3-双加氧酶（IDO）诱导和喹啉酸积累的副作用。
