高脂血症患者血清补体C3、C4、备解素和白细胞补体调节蛋白CD35、CD55、CD59的表达

目的:探讨高脂血症患者血清补体和外周血白细胞补体调节蛋白的表达及其在动脉粥样硬化中的意义。方法:选高脂血症患者46例(高脂血症组),年龄、性别、体重指数匹配的正常人20例作为正常对照组,用免疫散射比浊法测血清补体C3、C4、备解素(Pf);用流式细胞术测定外周血中性粒细胞、淋巴细胞和单核细胞CD35、CD55、CD59的表达,观察上述指标在高脂血症组中的变化,分析影响因素。结果:高脂血症组血清C3、C4、Pf水平较正常对照组明显升高(P<0.01);补体C3、C4水平与血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDLC)明显正相关(P<0.01),Pf与TC、LDLC正相关(P<0.01)。CD35阳性淋巴细胞、单核细胞、粒细胞百分率较正常对照组升高(P<0.05),CD35阳性淋巴细胞、粒细胞百分率与TG呈正相关(P<0.05～0.01);CD55阳性淋巴细胞平均荧光强度较正常对照组下降(P<0.05);CD59阳性淋巴细胞、单核细胞百分率较正常对照组下降(P<0.05)。结论:高脂血症患者血清补体C3、C4、Pf升高,白细胞补体调节蛋白表达改变,补体及补体调节蛋白的改变与血脂水平相关,表明脂代谢紊乱可影响补体及补体调节蛋白的表达,提示补体及补体调节蛋白可能参与动脉粥样硬化的病理生理过程。

Expression of Complement C3, C4, Properdin and Complement Regulatory Proteins CD35, CD55, CD59 in Dyslipidemic Patients

Objective:To investigate the serum level of complement C3,C4,properdin(Pf)and expression of complement regulatory proteins CD35,CD55,CD59 on leukocytes in dyslipidemia, and to explore the pathogenetic role of complement system in atherosclerosis. Methods:Serum C3,C4,Pf was tested with rate nephelometry and expression of CD35,CD55,CD59 on leukocytes were tested with flowcytometry in 46 patients with dyslipidemia,and 20 age-,sex-,BMI-matched healthy controls. The factors which might affect the expression of complement and complement regulatory proteins were investigated. Results:The serum levels of C3,C4,Pf in dyslipidemia patients were significantly higher than those in healthy controls(p<0.01). C3,C4 were positively correlated with TC,TG and LDL-C(p<0.01),and Pf was positively correlated with TC and LDL-C(p<0.01).In dyslipidemic patients,the percentage of CD35-positive lymphocytes and CD35-positive granulocytes positively correlated with TG(p<0.05)were increased(p<0.05).The mean fluorescence intensity of CD55 positive lymphocytes was lowered (p<0.05).The percentages of CD59 positive monocytes and lymphocytes were reduced(p<0.05). Conclusion:The serum C3,C4,Pf levels were increased and the expression of complement regulatory proteins on leukocytes was changed in dyslipidemia, suggesting that complement system is involved in atherogenesis.