目的探讨CD59基因在藻蓝蛋白(C—phycocyanin,CPC)抗动脉粥样硬化发生发展中的作用。方法将40只ApoE基因缺失(ApoE+)小鼠随机分为4组:对照组、CPC处理组、CD59处理组、CD59+CPC处理组。在高脂饮食同时进行药物干预。12周后.RT-PCR检测全血中CD59mRNA水平,Western blot检测组织中CD59蛋白表达量。检测血清生化指标,并取主动脉根部制作石蜡切片,HE染色观察动脉粥样硬化斑块形成情况。结果动脉粥样硬化小鼠模型构建成功。CD59与CPC都具有一定的降低血脂水平和抑制动脉粥样硬化发展的作用,并且两者联合作用比单独给药效果更显著。此外CPC能促进小鼠体内CD59基因的表达。结论CPC对ApoE+、鼠的抗动脉粥样硬化作用可能是通过促进体内CD59基因的表达,进而延缓或抑制了动脉粥样硬化的发生发展。
To evaluate the effects of CD59 gene in occurrence and development of atherosclerosis with presence of C-phycocyanin (CPC), 40 mice with ApoE gene deletion (ApoE+) recruited were randomly divided into four groups: control group, CPC treated group, CD59 treated group and CPC+CD59 treated group. All mice fed on high-fat diet, and were treated with drug intervention respectively. At the end of the 12^th week, CD59 mRNA level was determined by RT-PCR, and CD59 protein expression was detected by Western blot. Blood fat levels of mice were also determined, and aortic roots were taken out for observing the degree of atherosclerotic plaques formation. We found that both CPC and CD59 gene could lower blood fat level and inhibit atherosclerosis formation, and the combination of CD59 gene and CPC could more effective. In addition, CPC could promote the CD59 mRNA and protein expression, thus further inhibit the progress of atherosclerosis, which might be the mechanism of anti-atherosclerosis roles of CPC.