Klimov A N, Dokusova O K, Petrova-Maslakova L G, Loviagina T N, Nagornev V A
Vopr Med Khim. 1977 Nov-Dec(6):803-7.
Development of resistance to experimental atherosclerosis due to immunization of newborn rabbits with homologous fraction of beta- and pre-beta-lipoproteins was accompanied by increased oxidation of cholesterol to biliary acids and by accelerated excretion of cholesterol. The phenomenon appears to be caused by two mechanisms: 1 (cholesterol, occurring in the fraction of free lipoproteins "unblocked" by the antibody (immunzied animals), is more readily oxidized to biliary acids in liver tissue than cholesterol, occurring in the autoimmune complex "lipoprotein-antibody" (non-immunized animals)); 2) the enzymes and biological systems, responsible for elimination of cholesterol from an organism (oxidation to biliary acids, excretion with bile), are activated after immunization of the newborn animals by the lipoprotein fraction endriched with cholesterol.
新生兔用β-脂蛋白和前β-脂蛋白的同源部分进行免疫后，对实验性动脉粥样硬化产生抗性的过程中，伴随着胆固醇氧化为胆汁酸的增加以及胆固醇排泄的加速。该现象似乎由两种机制引起：1）（在抗体“解除阻滞”的游离脂蛋白部分（免疫动物）中存在的胆固醇，比在自身免疫复合物“脂蛋白-抗体”（未免疫动物）中存在的胆固醇，在肝脏组织中更容易氧化为胆汁酸）；2）负责从生物体中清除胆固醇（氧化为胆汁酸、随胆汁排泄）的酶和生物系统，在新生动物用富含胆固醇的脂蛋白部分免疫后被激活。
