脑型疟疾免疫病理机制的实验研究：肿瘤坏死因子的作用

本文以化学发光法（ＣＬ）、诱化学发光法（ＩＣＬ）、红细胞变形性（ＥＤ）检测等方法研究了感染伯氏疟原虫（Ｐｌａｓｍｏｄｉｕｍｂｅｒｇｈｅｉ）Ａｎｋａ株的ＢＡＬＢ／ｃ小鼠在注射重组肿瘤坏死因子（ｒＴＮＦ）以后引起脑型疟疾（ＣＭ）时其血浆中活性氧（ＲＯＳ）及相关自由基与ＥＤ及ＥＤ与ＣＭ间的关系。结果发现在ＣＭ出现时动物血浆中ＲＯＳ及相关自由基水平明显增高，ＥＤ明显降低。使用抗氧化剂可以明显改善上述过程而使ＣＭ发生率下降。作者认为，疟原虫感染时ＴＮＦ的过量产生可使宿主吞噬细胞释放大量ＲＯＳ及相关自由基，血浆中这些物质的大量聚集使红细胞变形能力受到破坏，这时红细胞在通过具有极丰富血循环的脑组织时在脑微血管内易于形成广泛性微拴塞，导致ＣＭ形成。

THE EXPERIMENTAL STUDY ON THE IMMUNOPATHOLOGICAL MECHANISM OF CEREBRAL MALARIA

In this paper, the relation between the levels of reactive oxygen species (ROS) and interrelated free radicals in the blood plasma of BA LB/c mice infected with Plasmodium berghei Anka and their erythrocytic deformability (ED), and the relation between ED and cerebral malaria(CM) incidence of these mice were studied by chemiluminescence(CL), induced CL(ICL) and laser diffraction methods. The results suggested that ED decreased with the increase of the levels of ROS and free radicals in blood plasma when these mice were suffering from CM. Antioxidants may restrain the course so obviously that they can reduce the CM incidence, The following conclusions were advanced in this paper: The excessive TNF produced in later stage of malaria may induce excessive ROS and free radicals from phagocytes,which may induce a decline in ED.When the erythrocytes circulate through the brain tissue where blood is sufficiently supplied, they were easily blocked and formed extensive plugs in the brain microvessels. As a result, the CM appeared in the malarias.