ApoE基因缺陷鼠免疫、血液稳态和抗氧化功能改变  

Changes of immune, haemostasis and anti-oxidation functions in ApoE gene deficiency mice

作　　者：李晖[1] 李可基[1] 张宝慧[1] 拾景达[1] 

机构地区：[1]北京大学第三医院运动医学研究所,北京100083

出　　处：《北京大学学报（医学版）》2001年第4期347-350,共4页Journal of Peking University:Health Sciences

基　　金：国家自然科学基金 (39770 813)资助&&

摘　　要：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Objective: To study influence of ApoE dysfunction on haemostasis, T cell subpopulations and metabolism of lipids and free radicals. Methods: ApoE gene knockout (ApoE0) mice were used as the subjects and the homogeneous mice of C57BL/6J as the control. Results: In comparison with control, TC, TG and LDL C levels were higher in ApoE0 mice ( P <0.05), and their HDL C level was only 20% of the control ( P <0.01); the activity detected was 18.3% higher ( P <0.05) for tPA and 19.6% lower ( P <0.01) for PAI, and the ratio of tPA/PAI was 55% higher ( P <0.01) in ApoE0 mice; the activity of thrombinogen, thrombin and plasmin increased by 54.2% ( P <0.01), 135% ( P <0.01) and 37.6% ( P <0.01) respectively, and plasminogen decreased by 24.3 ( P <0.01) in ApoE0 mice; T cell subpopulation of CD4 + and CD8 + in ApoE0 mice decreased by 17.2% ( P < 0.01) and 58.9% ( P <0.01) respectively, and the ratio of CD4 +/CD8 + increased by 146% ( P < 0.01); SOD of ApoE0 mice was 17.5% lower ( P <0.01) and MDA was 29.8 ( P <0.01) higher in plasma, while SOD decreased insignificantly ( P >0.05) and MDA increased by 99% ( P <0.01) inliver; there were no differences in SOD activity and MDA level between two groups ( P >0.05) Conclusion: ApoE dysfunction causes disturbance of lipid metabolism, hyperfunction of coagulation and fibrinolysis, change of proportion of T cell subpopulation and disorder of oxidation and antioxidation balance.

关 键 词：载脂蛋白E类 T淋巴细胞亚群 自由基 免疫 血液稳态 抗氧化功能 

分 类 号：Q343.1[生物学—遗传学]