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目的 :探讨载脂蛋白E(apoproteinE ,ApoE)功能障碍对脂质代谢、血液稳态、脾T淋巴细胞亚群及自由基代谢的影响。方法 :以ApoE基因缺陷 (ApoE0 )鼠为实验模型 ,以相同遗传背景的C5 7BL/ 6J鼠为对照 ,对比血浆中有关指标的不同。结果 :与对照组比较 ,ApoE0鼠的总胆固醇 (totalcholesterol,TC)、甘油三酯 (triglyceride ,TG)和低密度脂蛋白胆固醇 (lowdensitylipoproteincholesterol,LDL C)水平均高于正常对照鼠 (P <0 .0 5 ) ,而ApoE0鼠的高密度脂蛋白胆固醇 (highdensitylipoproteincholesterol,HDL C)仅为正常对照鼠的 1/ 5 (P <0 .0 1) ;ApoE0鼠的血浆组织纤溶酶原激活物活性 (tissueplasminogenactivatoractivity ,tPAa)增加 18.3 % (P >0 .0 5 ) ,纤溶酶原激活抑制剂活性 (plasminogenactivatorinhibitoractivity ,PAIa)下降 19.6 % (P <0 .0 5 ) ,使tPAa/PAIa升高 5 5 % (P <0 .0 1) ;ApoE0鼠的凝血酶原活性、凝血酶活性和纤溶酶活性分别升高 5 4.2 % (P <0 .0 1)、135 % (P <0 .0 1)和 37.6 % (P <0 .0 1) ,而纤溶酶原活性降低 2 4.3% (P <0 .0 1) ;ApoE0鼠CD4+和CD8+分别降低 17.2 % (P <0 .0 5 )和 5 8.9%(P <0 .0 1) ,CD4+/CD8+升高 146 % (P <0 .0 1) ;ApoE0鼠血浆超氧化物岐化酶 (superoxided
Objective: To investigate the effects of apoprotein E (ApoE) dysfunction on lipid metabolism, blood homeostasis, splenic T lymphocyte subsets and free radical metabolism. Methods: ApoE gene-deficient (ApoE0) mice were used as experimental models and the same genetic background of C5 7BL / 6J mice as controls, which compared the different indexes in plasma. Results: Compared with the control group, the levels of total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDL C) in ApoE0 mice were significantly higher than those in normal control mice (P <0. 0.05), while ApoE0 mice only had 1/5 of highdensity lipoprotein cholesterol (HDL C) in the normal control group; plasma tissue plasminogen activator activity in ApoE0 mice ( (P <0.05), the plasminogen activator inhibitor activity (PAIa) decreased by 19.6% (P <0.05), increased tPAa / PAIa by 55% (P <0.01). The prothrombin activity, thrombin activity and plasmin activity in ApoE0 mice increased by 5.22% (P <0.01), 135% (P <0.01) And 37.6% respectively (P <0.01), while the activity of plasminogen decreased by 23.3% (P <0.01). The CD4 + and CD8 + of ApoE0 mice decreased by 17.2% 8.9% (P <0.01), CD4 + / CD8 + increased 146% (P <0.01); superoxided ApoE0 mouse plasma superoxide dismutase