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罗格列酮对apoE基因敲除小鼠血清NOS/NO的影响 被引量:3

Effect of rosiglitazone on serum NOS/NO in apolipoprotein E knockout mice
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摘要 目的探讨罗格列酮对apoE基因敲除小鼠血清NOS/NO的影响。方法20只8周龄apoE基因敲除小鼠分为动脉粥样硬化(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10 mg.kg-1.d-1罗格列酮,12周后获取静脉血和主动脉标本。用硝酸还原酶法测定NO及NOS。用全自动生化分析仪测定血脂水平。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NO、NOS含量均显著低于正常对照组(P<0.05),罗格列酮干预组NO、NOS含量均显著高于模型组。结论罗格列酮具有抗AS作用,且其抗AS作用可能与其逆转受损的内皮细胞功能有关。 Objective To observe the effect of rosiglitazone on serum NOS/NO in apolipoprotein (apo) E knockout mice. Methods Twenty eight-week-old apoE knockout mice were intragastrically administrated 0.2 ml 5% sodium carboxymethycellulose for 12 weeks to establish the animal models of atherosclerosis, in which half of mice simultaneously received 10 mg ·kg^-1·d^-1 rosiglitazone as treatment. Ten wildtype mice were used as the normal control group. All mice were fed on normal chow diet. After 12 weeks, aorta were used for histomorphometric analysis by means of HE. Vessel blood was collected for plasma lipid, NO and NOS. Re- sults Histomorphometric analysis showed that the area of atherosclerosis plaque in mice receiving rosiglitazone was significantly smaller than the mouse models of atherosclerosis, while the plasm lipid, NO and NOS were higher. Conclusion Rosiglitazone can inhibit the development of atherosclerosis, which mechanism is related to the protection of vascular endothelial function.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2006年第11期1204-1205,共2页 Journal of Third Military Medical University
关键词 罗格列酮 动脉粥样硬化 APOE基因敲除小鼠 一氧化氮 一氧化氮合酶 rosiglitazone arteriosclerosis apoE-knockout mice NO NOS
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