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机构地区:[1]泰州市人民医院 [2]扬州大学医学院 [3]扬州大学
出 处:《黑龙江医药》2013年第5期774-777,共4页Heilongjiang Medicine journal
摘 要:目的:ApoE-/-小鼠,给予甘草总黄酮(GTF)干预,探索其调脂、抗氧化作用,进而研究其防治动脉粥样硬化(AS)形成的作用。方法:健康雄性ApoE基因敲除小鼠30只,9周龄,适应性饲养1周,随机分成5组:模型组;阳性对照(银杏叶片)组;GTF高、中、低剂量组,每组6只,分别给药。另取8周龄正常C57BL/6J小鼠6只为正常对照组(给予普通饲料喂养);正常对照组、模型组给以等容剂量生理盐水,连续干预4周。末次给药后次日处死小鼠,摘眼球取血,分离血清,检测相应指标;分离肝脏,制作切片,观察肝脏病理改变。结果:模型组血脂、脂质过氧化产物(MDA)、超氧化物歧化酶活力(SOD)、氧化性低密度脂蛋白(ox-LDL)水平及肝脏形态学显示造模成功。GTF高、中剂量可有效降低血清TC、TG、LDL-C,升高HDL-C水平,抑制MDA及ox-LDL形成,增强SOD活性,提高机体抗氧化能力,对AS发生发展有抑制作用。结论:14周龄ApoE-/-小鼠血脂水平异常,伴随氧化反应增强、抗氧化活力降低等反应,GTF通过调节血清脂质、脂蛋白胆固醇水平,亦可抑制氧化损伤减少ox-LDL的产生进而防止或延缓AS的形成。Objective:ApoE-/- mice were given licorice flavonoids (GTF) intervention, explore its lipid, antioxidant effect, and thus to study the prevention and treatment of AS formation mechanism. Methods: 30 healthy male ApoE knockout mice, 9 weeks old, adaptive feeding one week, were randomly divided into five groups: model group; positive control (Ginkgo biloba) group; GTF high, medium and low dose groups, administered separately. Another 8-week-old normal C57BL/6J mice as normM control group (given normal diet); nor- mal control group, model group given isovolumetrie normal saline, continuous intervention for 4 weeks. The day after the last administra- tion, the mice were killed, eyeball blood serum was separated, detected corresponding indicators; separation of the liver, making slices, observe pathological changes in the liver. Results: The model group lipids, lipid peroxidation (MDA), superoxide dismutase activity (SOD), oxidized low-density lipoprotein (ox-LDL) levels and liver morphology shows successful model. GTF high dose can effectively re- duce serum TC, TG, LDL, raise HDL levels, inhibit the formation of MDA and ox-LDL, enhanced SOD activity and increased antioxidant capacity, on the development of AS inhibition. Conclusion: 14-week-old ApoE-/- mice abnormal lipid levels, accompanied by oxida- tion enhanced antioxidant activity and decreased reaction, GTF by regulating serum lipids, lipoproteins, also inhibit oxidative damage to reduce the generation of ox-LDL and thus prevent or delay the formation of AS.
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