罗格列酮对apoE基因敲除小鼠血浆高敏C反应蛋白水平的影响

Effect of rosiglitazone on inflammatory factors in apolipoprotein E knockout mice

目的探讨罗格列酮对apoE基因敲除小鼠血浆炎症因子水平的影响。方法20只8周龄apoE基因敲除小鼠随机分为动脉粥样硬化(atherosclerosis,AS)模型组和罗格列酮干预组,另取10只8周龄野生型C57/BL小鼠作为正常对照组。3组均饲喂普通饮食,罗格列酮组给予10mg.kg-1.d-1,12周后获取静脉血和主动脉标本。分别用胶乳凝聚法、微量快速测定法及XO法测定高敏C反应蛋白(hs-CRP)、丙二醛(MDA)活性和超氧化物歧化酶(SOD)活性。HE染色后镜下观察主动脉病变。结果AS模型组主动脉形成明显的动脉粥样硬化斑块,罗格列酮干预组病变较AS组轻;AS组血浆MDA、hs-CRP含量均显著高于正常对照组,罗格列酮干预组MDA、hs-CRP含量均显著低于模型组。模型组血浆SOD含量活性明显低于正常对照组,而罗格列酮干预组活性显著高于模型组。结论罗格列酮具有抗AS作用,且其抗AS作用可能与其抗炎症相关。针对炎症有望控制AS的发生发展。

Objective To observe the effect of rosiglitazone on inflammatory factors in an apolipoprotein（apo）E knockout mouse model. Methods Eight-week-old apoE knockout mice were divided into rosiglitazone group（10 cases） and atherosclerosis（AS） group （10 cases）. Wildtype mice were used as normal control group（10 cases）. All mice were fed with normal chow diet. In addition to normal diet, rosiglitazone group received rosiglitazone 10mg/kg of body weight/d. After 12 weeks, aorta were used for histomorphometric analysis by means of HE. Vessel bloods were collected for plasma hs CRP,MDA and SOD. Results Histomorphometric analysis showed that the area of atherosclerosis plaque in rosiglitazone group was significantly smaller than that in AS group. The plasm hs-CRP and MDA in rosiglitazone group were significantly lower than those in AS group while the plasma SOD in rosiglitazone group was higher than that in AS group. Conclusion Rosiglitazone can inhibit the development of atherosclerosis. The mechanism is related to modulation of inflammatory factors. Anti-inflammation is a potential way for controlling atherosclerosis.