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目的： 为研究脑型疟发病机制及防治提供理论依据。方法： 应用十二烷基硫酸钠－聚丙烯酰胺凝胶电泳 （ＳＤＳ－ＰＡＧＥ） 技术， 对云南省１９ 例脑型疟患者感染红细胞 （ＰＥ） 表达的红细胞膜蛋白１（ＰｆＥＭＰ－１） 进行分析， 并分别与４３ 例恶性疟、９ 例间日疟患者ＰＥ表达的ＰｆＥＭＰ－１和ＰｖＥＭＰ－１及６ 例健康人红细胞膜蛋白（ＥＭＰ） 进行比较。结果： 脑型疟患者ＰＥ存在高表达的高分子量ＰｆＥＭＰ－１， 分子量为２６０～３２０ ｋＤａ。恶性疟及间日疟患者ＰＥ不表达２６０ ｋＤａ 以上的高分子量ＰｆＥＭＰ－１，分别测到分子量最大为２４０ｋＤａ 的ＰｆＥＭＰ－１和１８０ ｋＤａ的ＰｖＥＭＰ－１。健康人对照组ＥＭＰ分子量为１４０ ｋＤａ。结论： 脑型疟患者ＰＥ高表达的不同高分子量ＰｆＥＭＰ－１ ２６０～３２０ ｋＤａ， 与脑血管内皮细胞（ＥＣ） 不同受体蛋白ＣＤ３６、血小板反应蛋白 （ＴＳＰ）、细胞间粘附分子１ （ＩＣＡＭ－１）、血管细胞粘附分子１ （ＶＣＡＭ－１） 和内皮白细胞粘附分子１（ＥＬＡＭ－１） 及硫酸软骨素Ａ （ＣＳＡ） 的结合是脑型疟发病的分子基础， 可导致脑型疟患者发生昏迷。
Objective: To provide a theoretical basis for studying the pathogenesis and prevention of cerebral malaria. Methods: Erythrocyte membrane protein 1 (PfEMP-1) expressed in erythrocytes (PE) of 19 cases of cerebral malaria patients in Yunnan Province was analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) And compared with PfEMP-1, PvEMP-1 and 6 healthy human erythrocyte membrane protein (EMP) in 43 cases of P. falciparum and 9 cases of P. falciparum PE, respectively. Results: There was high expression of PfEMP-1 in PE with a molecular weight of 260-320 kDa. Plasmodium falciparum and Plasmodium vivax did not express PfEMP-1 with a molecular weight above 260 kDa, and PfEMP-1 with a molecular weight of 240 kDa and PvEMP-1 with 180 kDa were measured respectively. The healthy human control group had a molecular weight of 140 kDa. Conclusion: The expression of PfEMP-1 with high molecular weight (PfEMP-1) between cerebral malaria patients with high expression of PE and CD36, TSP, ICAM-1 -1), vascular cell adhesion molecule 1 (VCAM-1) and endothelial cell adhesion molecule 1 (ELAM-1) and chondroitin sulfate A (CSA) are the molecular basis of cerebral malaria pathogenesis, Malaria in a coma.